ABSTRACT. Prostate cancer (PCa) continues to be one of the leading non-communicable diseases worldwide, the development of PCa is increasingly attributed to the combination of essential & toxic elements. This article reviews current epidemiology, mechanisms, and analytical data regarding the role of Zinc (Zn); Selenium (Se); copper (Cu); Cadmium (Cd); Arsenic (As); Lead (Pb); and many other trace elements in pathology related to PCa. Essential elements such as Zn and Se promote antioxidant defense systems, DNA repair & apoptosis, and metabolism of Citrate, while toxic metals like Cd, As, Pb, and excessive Cu increase the incidence of oxidative stress, endocrine dysfunction, genomic instability, and inflammation associated with PCa initiation and progression. The importance of multi-element Interactions, particularly antagonistic interactions such as Zn & Cd or Se & As is emphasized when developing exposomic strategies for evaluating mixture-factor effects.
Advances in the use of IS-MS for non-invasive biomonitoring of hair and nails provide a reliable method for determining the long-term effects of multiple trace elements in different geographical areas. It has been demonstrated that the elemental imbalance associated with the development and aggressiveness of PCa depends on the geographical context. The data obtained confirm the need to integrate environmental exposure profiles with cellular and molecular pathways to improve prevention strategies, develop more accurate disease biomarkers, and implement effective public health measures. New approaches to diagnosis are needed, as well as technologies for early risk detection and prevention of PCa that are accessible to developing countries.Advances in the use of IS-MS for non-invasive biomonitoring of hair and nails provide a reliable method for determining the long-term effects of multiple trace elements in different geographical areas. It has been demonstrated that the elemental imbalance associated with the development and aggressiveness of PCa depends on the geographical context. The data obtained confirm the need to integrate environmental exposure profiles with cellular and molecular pathways to improve prevention strategies, develop more accurate disease biomarkers, and implement effective public health measures. New approaches to diagnosis are needed, as well as technologies for early risk detection and prevention of PCa that are accessible to developing countries.
KEYWORDS: prostate cancer, trace elements, zinc, selenium, cadmium, arsenic, copper.KEYWORDS: prostate cancer, trace elements, zinc, selenium, cadmium, arsenic, copper.
For citation: Hussain M.B., Zaidi K., Lapin I.I., Lyapunovsky D.M., Skalny A.V., Bezrukov E.A., Torshin V.I., Severin A.E. The role of essential and toxic elements in the development of prostate cancer: comprehensive analysis and prospects. Report 1. Biological aspects. Trace elemets in medicine. 2026;27(1):13-23. DOI: 10.19112/2413-6174-2026-27-1-13-23
PROSTATE CANCER: SCOPE, BURDEN AND ETIOLOGIC INSIGHTS
Prostate cancer has become the most common cancer diagnosis in men and remains one of the most common to cause morbidity and mortality in older men. Globally, there is great variability in the incidence and mortality rate of PCa and this is partially due to differences in population screening, demographics, environmental and lifestyle factors (Bergengren et al., 2022; Crocetto et al., 2023). While age, family history and race/ethnicity are the most frequently documented risk factors of prostate cancer, the hereditary breast and ovarian cancer genes BRCA2 and HOXB13 are included as part of the greatest number of risk factors but do not account for the wide disparities seen throughout the world in terms of incidence rates, stage of diagnosis, and disease aggressiveness of prostatic carcinoma (Rawla, 2019; Pang et al., 2025). This has led to investigations over the past decade on PCa modifiable environmental risk factors.
Currently, the prolonged chronic effect of both toxic (Cadmium, Lead, Arsenic, and Mercury) and essential (Zinc, Selenium, and Copper) trace elements on PCa pathology has become biologically plausible. This is due to the role of these elements in redox regulation, DNA repair, hormonal action, and immune response (Górska et al., 2024; Zhou et al., 2025). An extensive systematic review and meta-analysis of trace elements levels in the serum of patients with PCa notes that those with PCa had homeostatic imbalances of Selenium (Se) and copper (Cu), with significantly lower Se levels and higher Cu levels when compared to controls. (Devi et al., 2025). Tshoni et al. (2024) even more integrated and expanded in their mechanistic review of trace metals and PCa, and stated that zinc (Zn) and Se deficiencies coupled with greater exposures to cadmium (Cd), arsenic (As), nickel (Ni), and lead (Pb), may disrupt genomic stability and epigenetic regulation and the transcriptomic and proteomic network of prostate tissue.
In recent study it was evaluated that several metals in tissue, urine, and serum of patients with PCa, noted the presence of Cd and As in higher amounts in the cancerous compared to the non-cancerous adjacent tissue (Tyagi et al., 2023). Also related data from Nigeria, suggesting that among men, higher urinary Cd was linked with PCa (adjusted OR ~2.5 per ten-fold increase), which was modified by Zn status and was strongest among men in the bottom quartile for Zn status (Bede-Ojimadu et al., 2023).In recent study it was evaluated that several metals in tissue, urine, and serum of patients with PCa, noted the presence of Cd and As in higher amounts in the cancerous compared to the non-cancerous adjacent tissue (Tyagi et al., 2023). Also related data from Nigeria, suggesting that among men, higher urinary Cd was linked with PCa (adjusted OR ~2.5 per ten-fold increase), which was modified by Zn status and was strongest among men in the bottom quartile for Zn status (Bede-Ojimadu et al., 2023).
Additionally, recent investigations have provided a detailed reassessment of the role of Se in PCa, highlighting the intricate relationship between Se status, selenoprotein function, and tumor biology. According to Jiang et al. (2023), observational studies have consistently suggested an inverse association between Se levels and PCa risk, implying that adequate Se intake may contribute to prevention or slower disease progression. However, large-scale randomized controlled trials evaluating Se supplementation have yielded conflicting results, indicating no significant protective effect against PCa (HR ≈ 0.95; 95% CI: 0.80–1.13). This proves the relationship’s complexity due to variations in Se dose, chemical form and timing of intake, interactions with other trace elements, and selenoprotein genetic polymorphisms. Moreover, supplementation may not account for the biologically active context of endogenous exposure to Se, which reiterates the need to examine the context of Se for possible cancer prevention and treatment (Jiang et al., 2023).
After above discussion, the evidence presents a balanced argument where trace elements exposures, i.e., low exposures to protective elements and high exposures to toxic metals, could be suspected to contribute to cancer and PCa cancer progression. This could, to an extent, account for some of the variation in disease burden related to cancer in different regions and populations. Nonetheless, the evidence heterogeneity, the challenges to assess exposure and the possible genetic or dietary moderator complexity, raise the necessity of new research involving stronger designs, exposure assessment and mechanistic studies in this field.
BIOLOGICAL IMPORTANCE OF TRACE ELEMENTS IN PROSTATE CANCER DEVELOPMENT
The prostate has a distinct method of handling metals, specifically Zn, among other metal ions, in connection to prostate cancer. Zn has a role in apoptosis (cell death) and proliferation within prostate cancer growth, the prostate processes citrate and stores Zn; when Zn is deficient in the prostate, this perturbation of normal apoptosis can lead to excessive proliferation of prostate cells. In other words, Zn deficiency is thought to be a factor in the uncontrolled proliferation of cancerous prostate cells (Karunasinghe, 2022; Shahrokhi et al., 2024). Se deficiency causing unregulated oxidative DNA damage and redox imbalance leads to uncontrolled cell proliferation, and, in addition, assists in the establishment of other cancer hallmarks. On the other hand, Castrate-resistant prostate cancer (CRPC), Cd and As, cause oxidative stress, contributed to epigenetic reprogramming, and alteration of metalloproteins with the maze of oxygen (Zhan et al., 2025). All these highlighted characteristics make Cd pro-carcinogenic in the experimental settings. Apart from the uncharacteristic attributes of other trace elements, Cd exposure correlates to higher risk of developing PCa in epidemiological studies (Devi et al., 2024).
Like uncharacterized attributes of Cu, Fe also poses troubling pro-carcinogenic attributes. Dysregulated Fe compounds reactive species, angiogenesis, and cell proliferation (Bede-Ojimadu 2023). Interactions among uncharacterized bio-elements that function as both "essential" (e.g., Zn and Se) and "toxic" (e.g., Cd, As, and excess amounts of Cu and Fe) provide significant mechanistic information for the way in which the potential development of PCa can be initiated by these bio-elements.
A review and meta-analysis by Devi have determined that Cu levels in serum of PCa patients was found to be significantly greater and Se was found to be lower in comparison with the control group (SMD = +1.85 Cu; SMD = –2.45 Se) showing that elements in the body changed during the disease process (Devi et al., 2025). Another important review concerning Zn and PCa stated, Zn levels in both the serum (SMD of –1.11) and prostatic fluid/tissue (SMD –3.70) were significantly lower, thus suggesting that Zn deficiency is a constant attribute in PCa (Shahrokhi et al., 2024). In a case-control study done on Nigerian men, each increase of ten times urinary Cd concentration was connected to a disease adjusted odds as significant as 2.53, and men with a lower portion of Zn had even stronger connection of 8.46 (Bede-Ojimadu et al., 2023). Cd and As concentrations were measured and find greater in tumor tissue than in non-tumor tissue and even adjacent non-tumor tissue (Karunasinghe et al., 2022).
Mechanisms of actions include the removal of Zn, loss of apoptotic restraint and cellular shift to glycolysis, proliferation metabolism; loss of Se encourages loss of redox homeostasis and impairs DNA repair; Cd sharing Zn binding sites, disrupting Zn cellular proteins, miRNA dysregulation, and hormonal pathway mimicry; Cu and Fe promoting Relative Oxygen Species (ROS) for proliferation and angiogenesis (Tshoni et al., 2024). In summary, uncontrolled trace elements physiology comprising deficiency of protective and exposure to metallotoxicity unfolds dysregulation and factors of disparate burden of PCa. To be able to help advance these findings into preventative or therapeutic strategies, further longitudinal studies with a focus on exposure assessment, multi metal interaction modelling, and integrating genetic and epigenetic controls is necessary.
POTENTIAL BIOLOGICAL PATHWAYS LINKING TRACE ELEMENTS TO PROSTATE PATHOLOGY
Pathogenesis of PCa is complicated by genetic, hormonal and environmental factors; within these complexities, trace elements (both essential and toxic) are being evaluated mechanistically. As discussed by Tshoni et al., essential and toxic metals modulate prostate carcinogenesis through mechanisms including oxidative stress, DNA damage, inflammation, hormone interference, and disruption of metal homeostasis (Tshoni et al., 2024).
Oxidative Stress and DNA Damage. One of the most documented ways that trace elements may influence prostate disease is through oxidative stress which leads to DNA damage. Redox-active metals (e.g. Fe, Cu, As, Cd) can catalyze the formation of reactive oxygen species (ROS), which can lead to base damage (e.g., 8-oxo-2′-deoxyguanine), single-strand or double-strand breaks in DNA. For instance, Pizent et al. (2022) showed correlations between blood Cd and Hg levels and oxidative stress markers in men with PCa, suggesting a relationship between metal burden and the initiation of oxidative stress. Likewise, Tyagi et al. (2023) determined the Cd and As levels were greater in PCa patients compared to controls, furthering support for toxic metal exposure driving oxidative insults in prostate tissue.
Oxidative stress not only initiate carcinogenic changes through mutagenesis, but could also be associated with tumor progression through contributions to genomic instability. Therefore, accumulation of oxidative DNA lesions may overwhelm repair pathways and promote selection of cells that grow better with DNA damage (Pizent et al., 2022). Thus, biomarker measurement of 8-oxo-dG, lipid peroxidation products (e.g., malondialdehyde, 4-HNE), or altered antioxidant enzyme activities (e.g., SOD, GPx) in conjunction with metal exposures may provide mechanistic linkage between exposure and pathology of the prostate (Kanwal et al., 2012).Oxidative stress not only initiate carcinogenic changes through mutagenesis, but could also be associated with tumor progression through contributions to genomic instability. Therefore, accumulation of oxidative DNA lesions may overwhelm repair pathways and promote selection of cells that grow better with DNA damage (Pizent et al., 2022). Thus, biomarker measurement of 8-oxo-dG, lipid peroxidation products (e.g., malondialdehyde, 4-HNE), or altered antioxidant enzyme activities (e.g., SOD, GPx) in conjunction with metal exposures may provide mechanistic linkage between exposure and pathology of the prostate (Kanwal et al., 2012).
Disruption of DNA Repair & Chromatin Regulation. In addition to adverse effects on direct DNA, trace elements potentially interfered with DNA repair systems and epigenetic regulation. For example, Zn is a structural component of several DNA-binding and repairing proteins; depriving Zn may disrupt these systems. In his mini review, Karunasinghe (2022) highlighted the role of Zn in prostate health and suggested altered Zn homeostasis may lead to an impaired DNA repair in prostate cells. Cd can substitute for Zn in Zn-binding proteins, impairing their activity and disrupting epigenetic regulation. These disruptions may lead to altered chromatin structure, leading to aberrant gene expression, both of which are indicators of carcinogenicity. Furthermore, the studies by Tshoni et al. (2024) suggest that the metal-dependent enzymes and epigenetic modifiers may facilitate the transition from exposure to malignant change in the prostate.Disruption of DNA Repair & Chromatin Regulation. In addition to adverse effects on direct DNA, trace elements potentially interfered with DNA repair systems and epigenetic regulation. For example, Zn is a structural component of several DNA-binding and repairing proteins; depriving Zn may disrupt these systems. In his mini review, Karunasinghe (2022) highlighted the role of Zn in prostate health and suggested altered Zn homeostasis may lead to an impaired DNA repair in prostate cells. Cd can substitute for Zn in Zn-binding proteins, impairing their activity and disrupting epigenetic regulation. These disruptions may lead to altered chromatin structure, leading to aberrant gene expression, both of which are indicators of carcinogenicity. Furthermore, the studies by Tshoni et al. (2024) suggest that the metal-dependent enzymes and epigenetic modifiers may facilitate the transition from exposure to malignant change in the prostate.
Endocrine or Hormonal Modulation. The prostate is regulated by hormones and is sensitive to androgens; therefore, metals that mimic or interfere with steroid metabolism may affect prostate carcinogenicity. For example, Cd has been described as a "metallo-estrogen" that can mimic estrogenic action or disrupt androgen receptor signalling. This disruption may lead to proliferation of prostate cells. As described by Tshoni et al. the endocrine disruption pathway is a potential mechanism linking trace metal exposure and pathogenesis of prostate tumors (Tshoni et al., 2024). Integrating such biomarkers as androgen receptor expression, testosterone/dihydrotestosterone ratios, and circulating hormones with trace elements may elucidate this pathway.Endocrine or Hormonal Modulation. The prostate is regulated by hormones and is sensitive to androgens; therefore, metals that mimic or interfere with steroid metabolism may affect prostate carcinogenicity. For example, Cd has been described as a "metallo-estrogen" that can mimic estrogenic action or disrupt androgen receptor signalling. This disruption may lead to proliferation of prostate cells. As described by Tshoni et al. the endocrine disruption pathway is a potential mechanism linking trace metal exposure and pathogenesis of prostate tumors (Tshoni et al., 2024). Integrating such biomarkers as androgen receptor expression, testosterone/dihydrotestosterone ratios, and circulating hormones with trace elements may elucidate this pathway.
Inflammation and Immune Regulation. Chronic metal exposure can also result in chronic inflammation, increased pro-inflammatory cytokines (e.g., IL-6, TNF-a) and alterations in the local prostate ecosystem that facilitate tumor growth. Metals, such as As, Cd or Pb, may initiate cytokine shifts and trigger macrophage activation to produce reactive nitrogen species to create an inflamed pro-tumor microenvironmental. The inflammation of the prostate might then enable malignant transformation or progression, especially in older men with latent prostate disease. Recently published mechanistic reviews emphasized inflammation as one of the connected pathways that metals promote prostate pathology (Tshoni et al., 2024).Inflammation and Immune Regulation. Chronic metal exposure can also result in chronic inflammation, increased pro-inflammatory cytokines (e.g., IL-6, TNF-a) and alterations in the local prostate ecosystem that facilitate tumor growth. Metals, such as As, Cd or Pb, may initiate cytokine shifts and trigger macrophage activation to produce reactive nitrogen species to create an inflamed pro-tumor microenvironmental. The inflammation of the prostate might then enable malignant transformation or progression, especially in older men with latent prostate disease. Recently published mechanistic reviews emphasized inflammation as one of the connected pathways that metals promote prostate pathology (Tshoni et al., 2024).
Interference with essential metalls Homeostasis. Trace elements pathology in the prostate includes disturbances of essential metallic homeostasis, in particular Zn and Se. Zn is uniquely concentrated in the normal prostate and facilitates citrate metabolism, regulation of cell-apoptosis, and antioxidant defences. With disturbed Zn homeostasis due to deficiency, or displacing it with Cd, prostate cells lose critical inhibitory control over proliferation and apoptosis (Karunasinghe, 2022; Tshoni et al., 2024) Se is central to antioxidant protection and DNA repair when incorporated into selenoprotein (e.g., glutathione peroxidases), and its deficiency or dysregulation has been implicated in prostate tumourigenesis (Jiang et al., 2023; Tshoni et al., 2024). Therefore, a high toxic metal burden may not only exert direct damage, but also deplete protective elements from tissues, resulting in an additive elevation of risk.Interference with essential metalls Homeostasis. Trace elements pathology in the prostate includes disturbances of essential metallic homeostasis, in particular Zn and Se. Zn is uniquely concentrated in the normal prostate and facilitates citrate metabolism, regulation of cell-apoptosis, and antioxidant defences. With disturbed Zn homeostasis due to deficiency, or displacing it with Cd, prostate cells lose critical inhibitory control over proliferation and apoptosis (Karunasinghe, 2022; Tshoni et al., 2024) Se is central to antioxidant protection and DNA repair when incorporated into selenoprotein (e.g., glutathione peroxidases), and its deficiency or dysregulation has been implicated in prostate tumourigenesis (Jiang et al., 2023; Tshoni et al., 2024). Therefore, a high toxic metal burden may not only exert direct damage, but also deplete protective elements from tissues, resulting in an additive elevation of risk.
From Initiation to Progression and Treatment Response. These pathways oxidative stress, DNA damage, hormonal disruption, inflammation and essential metal imbalance function along the tumor initiation, but also along its progression. For example, the patterns of trace elements may affect tumor aggressiveness (Gleason score), metastatic potential, or response to treatment (e.g. radiotherapy, androgen-deprivation therapy) by modifying tumor microenvironmental, DNA repair capacity, or antioxidant capacity (Neslund-Dudas et al., 2018; Tshoni et al., 2024). So, a detailed exposure mapping, in combination with biomarkers and clinical or pathologic data (e.g. stage, Gleason grade, PSA kinetics), may provide an opportunity to identify high-risk individuals, prognostic biomarkers, or novel intervention avenues (Lim et al., 2019).
CURRENT EPIDEMIOLOGIC EVIDENCE LINKING TRACE ELEMENTS AND PROSTATE CANCER
There have been breakthroughs in trace elements epidemiology that focus on the epidemiological elemental factors of prostate carcinogenesis, though establishing causality is still difficult. Cd is cited as one of the most studied environmental carcinogens (IARC, 2012). Multiple meta-analyses and population-based studies pointed out the relationship of Cd to the increase in risk of PCa due to its pro-oxidant and endocrine-disrupting characteristics. Firmani et al., (2024) updated meta-analyses that showed chronic exposure to Cd is correlated to increases in risk of developing PCa, although there is still some heterogeneity in the exposure assessments. Mohammadian-Hafshejani and colleagues (2024) provide further evidence to support the relationship between Cd and PCa. With increasing levels of Cd exposure, the risk of developing PCa is also increasing, which adds to the biological support of the potential for Cd to cause prostate cancer. At the population level, Bede-Ojimadu et al. (2023) observed that among Nigerian men, urinary Cd was strongly associated with PCa incidence, particularly in individuals with low Zn status, suggesting a toxic-nutrient interaction antagonism between Cd and Zn.
There are still mechanistic and epidemiologic ties with As exposure due to it being the carcinogenic agent as well (IARC, 2012). Dennis et al. (2024) describes toenail concentrations of inorganic As were positively associated with PCa among pesticide applicators, which reinforces the idea of long-term As exposure as a potential driver of prostate carcinogenesis. In a recent study, Tyagi et al. (2023) showed how serum As and Cd levels were higher in PCa patients than in the controls, validating the association between toxic metal burden and the advancing stage of the disease.
One the other hand, the association of the other essential elements, particularly Se and Zn are complex and contextual. Quoting multiple experimental and clinical studies, Jiang et al. (2023) showed that Se, via its Selenoprotein constituent, possesses potent antioxidant and anti-inflammatory properties that may avert the onset of a tumor. Still, in a meta-analysis, Devi et al. (2025) noted epidemiological findings were contradictory. For instance, serum Se levels that were extremely low, and conversely, very high were associated with PCa. Zn plays a major role in the prostate and is the predominant constituent of the normal prostatic epithelium, and in citrate metabolism and apoptosis (Karunasinghe, 2022). However, epidemiological and clinical studies on the relationship between Zn status and PCa still show inconsistent results. Shahrokhi et al. (2024) reported that while malignant prostate tissue lacked Zn, circulating Zn levels inconsistent predictors of risk, likely due to disease-related redistribution rather than an absence of Zn in the diet.
Recent multi-elemental study by Zhan et al. (2025) profiled 19 elements among PCa patients in Southwest China and found complex, integrated patterns of dysregulation involving Cd, Cu , Fe, and Se, underscoring the importance of modeling mixtures. Similarly, Tshoni et al. (2024) found that oxidative stress, inhibition of DNA repair, and hormonal disruption, all of which are mediated by metals, integrated together in PCa pathogenesis. Overall, the multiple studies demonstrate the element-specific heterogeneity, dynamics in co-exposure, and context with respect to host nutrition or genetics are what likely account for the relationships observed involving trace elements calling for improved multi-element exposure assessment, biomarker validation, and integrative approaches to epidemiological research, in order to disentangle the contributions of trace elements to the etiology of PCa.
REGIONAL CONTEXT
The different environmental, industrial, and dietary contexts of Russia and other countries provide a reason to compare the roles of trace elements in the pathogenesis of PCa in different countries. Although different regions face environmental metal contamination, the sources, intensity, and population exposures differ greatly, giving the regions a unique opportunity to explore the consequences of trace elements and their interactions on the prostate.
Russia shows a unique distribution of metals particularly in proximity to industrial and mining regions (Skalny et al., 2015). Evidence has shown elevated accumulation of toxic metals and great concern with mining and metallurgical regions impacting local people (Kirichuk et al.,2023; Grabeklis et al., 2020). Russian biomonitoring studies showing exposures to Cd, Pb, and mercury (Hg) across space, related to regional contamination from industrial emissions and legacies from prior pollution (Skalny et al., 2023). This is advanced use of keratin-based biomarker and aligns with exposomic approaches that are needed in Europe (Shilnikova et al.,2023). Furthermore, Russian studies has commenced looking into the use of multi-elemental and mechanistic strategies to study the combined effects of metals Signatures on a broader scale. This will improve our overall understanding of how to link actual metal exposures to the development of PCa risk. (Grabeklis et al., 2020; Tshoni et al., 2024).
Studies focus on the East Asia indicate the incidence of prostate cancer is increasing and suggests that the combined exposure of trace and heavy metals may be the main contributing factor (Pang et al., 2023; Jiang et al., 2025). A case-control study from Zhan and fellow conducted in Southwest China which used ICP-MS to quantify 19 serum elements, found that prostate cancer correlated with lower copper, zinc, and selenium levels as well as altered inter-element correlations, which further demonstrates the importance of multi-element panels for targeted biomonitoring (Zhan et al., 2025). Both increasing evidence of population studies and mechanistic studies of PCa are showing that exposure to a combination of heavy metals can affect certain pathways and cancer-related genes. Through an epidemiological study, metal-responsive cancer driver genes have been found (Song et al., 2025; Jiang et al., 2023). These studies underscore the need for combined exposure analysis and transcriptomic studies in certain areas. PCa is increasingly prevalent in China, and is further complicated with complicated region-specific patterns of certain multi-element combinations in serum and tissue that probably reflect industrial activities, mining, metallurgy, coal burning, and selenium in diet.
While in South Asia, Pakistan’s unregulated industrialization, unregulated effluent discharges, and over-usage of agro-chemicals have raised soil and water contamination levels with Cd, Pb, As, and chromium (Cr). The shallow aquifers of Punjab and Sindh regions have been documented with As, which can have long-term carcinogenic consequences (Shahid et al., 2023). Aziz et al. (2023) documented Cr bioaccumulation in the aquatic fauna of Central Punjab and highlighted the risk of chronic exposures to humans. Hussain et al. (2023) conducted a cross sectional study and reported biomarker levels of Cd, Pb, and Ni in the hair and blood of men, particularly industrial and agricultural workers from Southern Punjab, confirming ongoing environmental exposure. Qayyum et al. (2025) also built on this work by looking into serum levels of 20 metals in male patients with prostate diseases and showed significant associations of elevated Cd, Ni, and Pb levels with prostate gland pathology, while Zn and Se appeared to offer protection. The imbalance of toxic-essential metals represents a mechanistic area of focus. Research by Chanihoon et al. (2022) from Pakistan showed that Zn deficiency and Cd exposure increased oxidative damage and DNA instability in breast cancer, a mechanism that can be expected for PCa as well.
Studies show that prostate cancer in the Middle East and Gulf region is often diagnosed at an advanced stage, with many men presenting with metastatic, high‑PSA disease and rapid progression from castration-sensitive to castration‑resistant states. A multicenter retrospective study comprised of 615 men over 4 countries was published by El-Karak and co-workers. Slightly more than half of them had metastatic disease. Metastatic castration sensitive diseases had higher mean PSAs than the localized disease and the time intervals between mCSPC and Castration Resistance and between mCRPC and the next line of therapy were short (El-Karak et al., 2024). Alasker and co-authors in Saudi Arabia Analytic Description of the National Registry reported more frequent elevated PSAs and advanced disease stage at the time of diagnosis and marked regional variation in the incidence and mortality statistics which probably correlate to the variation in the ecosystem, diet, occupation, and access to healthcare (Alasker et al., 2023).
Supporting the clinic and the registry, Kearney et al. had analyzed the data from the Global Cancer Observatory and reported from several countries in the world which do not belong to the Gulf region that the age standardized incidence and mortality rates were significantly variable and that the ratio of the mortality to incidence was high suggesting that the diseases in such countries were quite aggressive and the disease is at an advanced stage at the time of diagnosis (Kearney et al., 2023). The studies show how most patients in the region are diagnosed late, suffer high PSA, and have varying signs and symptoms, which is the situation in the Middle East and Gulf region and will aid in understanding the epidemiology of how essential and toxic trace elements may relate to the risk and progression of prostate cancer in conjunction with genetics, lifestyle and healthcare system factors in the future.
Comparatively different countries have common exposures, though their contexts are different. In Pakistan, the problems mainly relate to As in groundwater and Cd in foods, while in Russia, the problems mainly relate to industrial wastes and metallurgical wastes. In addition, dietary factors also modify metal intake; for example, while some parts of Russia consume a lot of Se from the seafood, the diet in Pakistan is almost entirely based on cereals, which have lower Se concentrations. Together, these regions illustrate how the risk PCa and its progression are influenced by differing metal mixtures, deficiencies, and exposures. While China reports dysregulations across multiple elements due to industrial emissions and variable selenium in the diet. The Gulf States show high incidence and mostly late-stage disease which suggests the role of uninvestigated environmental metals, diet, and disease in advancing clinical stages of the disease.
Prostate cancer patterns across Russia, China, Gulf States, and Pakistan demonstrate the importance of differentiated environmental and industrial metal exposures shaping bio-elements disease relationships. Tyagi et al. (2023) argued that environmental and dietary contexts can alter the internal dose of trace elements and their influence on the disease phenotype. These findings are supported by global studies highlighting the extent that Zn–Cd antagonism is important to PCa biology (Bede-Ojimadu et al., 2023; Firmani et al., 2024). The protective effect of Se is dependent not only on antioxidant selenoprotein, but by the local soil and dietary patterns; the Se deficiencies common in South Asia may impair redox homeostasis (Jiang et al.,2023; Petukhov et al., 2018).Prostate cancer patterns across Russia, China, Gulf States, and Pakistan demonstrate the importance of differentiated environmental and industrial metal exposures shaping bio-elements disease relationships. Tyagi et al. (2023) argued that environmental and dietary contexts can alter the internal dose of trace elements and their influence on the disease phenotype. These findings are supported by global studies highlighting the extent that Zn–Cd antagonism is important to PCa biology (Bede-Ojimadu et al., 2023; Firmani et al., 2024). The protective effect of Se is dependent not only on antioxidant selenoprotein, but by the local soil and dietary patterns; the Se deficiencies common in South Asia may impair redox homeostasis (Jiang et al.,2023; Petukhov et al., 2018).
PUBLIC HEALTH AND CLINICAL RELEVANCE
The implications of recent findings on trace elements and the development of PCa are significant for the risk of public health, preventive oncology, and clinical management. Studies show that imbalances (deficiency and excess) of certain trace elements may alter the risk, aggressiveness, and response of the disease to treatment (Devi et al., 2025; Tyagi et al., 2023; Tshoni et al., 2024). There are specific elemental signatures including elevated levels of Cd and Pb and lower levels of Zn and Se, which are strongly correlated with PCa. Findings of this nature call for translation across the environmental, nutritional, and clinical spectra.
The metal-induced carcinogenesis perspective justifies the tightening of rules concerning industrial emission controls, the composition of agrochemicals, and the management of mining waste. The need for such action is illustrated with evidence from multiple countries. Hussain et al. (2023) showed that southern Punjab, in Pakistan, had a male population with highly elevated Cd, Pb, and As levels, whereas in Russia (Skalny et al., 2015), Kirichuk et al. (2023) documented similar multi-element exposures in mining-affected regions. Such findings are similar to those from Nigeria, where there is an association between Cd exposure and increased risk of PCa, especially in the context of Zn deficiency (Bede-Ojimadu et al., 2023). These findings underscore the need for metal burden-inspired disease etiology research to guide localized, exposure-focused mitigation policies (Laoye et al., 2025; Shahid et al., 2023).
From a clinical standpoint, trace elements like Zn and Se represent possible biomarkers and modulators of prostate tumor biology. Part of Selenium's antioxidant role is performed by selenoprotein, which may prevent oxidative DNA damaging, and progression of Serelated metabolites PCa has been documented (Jiang et al., 2023). Additionally, Zn induces apoptotic processes, and its depletion prevents citrate metabolism in prostate tissue facilitating its transformation (Karunasinghe, 2022; Shahrokhi Nejad et al., 2024). Multiple-element analysis, like those performed by Zhan et al. (2025) and Qayyum et al. (2025), demonstrated that co-exposures, rather than deviation from single-elements, are better predictors of PCa incidence and severity. This advocates the construction of exposure derived risk models incorporating nutritional and toxico-logical elements (Firmani et al., 2024; Coradduzza et al., 2025).
Non-invasive biomonitoring tools like hair and nail analysis for elemental composition provide new means for surveillance of exposure and screening at the population level. Implemented laser ablation and new spectroscopic methods provide accurate multi-element assessments (Chan et al., 2023; Skalny et al., 2023 ; Silva et al., 2025;). These methods are most advantageous in under-resourced areas of the world lacking environmental monitoring (Tehrani et al., 2020; Batyrova et al., 2025). The designed epidemiologic studies and early detection programs would benefit from these methods by enabling longitudinal studies of the exposure–response relationships in populations.
Incorporating dietary suggestions focused on essential micronutrient consumption rates and quotient levels to combat the oxidative and inflammatory effects of toxic metals is necessary for public health responses (Saleh et al., 2020; Pizent et al., 2022). Mechanistic insight from Hussain et al. (2024) demonstrates how pollution-induced changes in the bioavailability of certain trace elements lead to oxidative stress and systemic inflammation, both of which are closely associated with the development of PCa. In addition to prevention, exposure-linked metabolic and genomic biomarkers may position malignancy chemopreventive and therapeutic strategies to target PCa redox and metal-regulated pathways (Tshoni et al., 2024).
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Information about the authors:
Muhammad Bakir Hussain – Post-graduate Student, Centre for Bioelementology and Human Ecology
ORCID: 0009-0007-5425-9180
Kamran Zaidi – Associate Professor, Department of Urology
ORCID: 0009-0006-9168-5210
Ilya I. Lapin – Laboratory Assistant, Laboratory of Molecular Dietetics,
Centre for Bioelementology and Human Ecology;
Assistant of Department of Medical Elementology
ORCID: 0009-0005-5176-9770; SPIN: 5281-1047
Dmitry M. Lyapunovsky – Apprentice-Researcher
at the Laboratory of Medical Elementology and Human Ecology
of the Research Institute of Molecular and Cellular Medicine of Medical Institute,
Post-Graduate Student of Department of Medical Elementology of Medical Institute
ORCID: 0009-0003-4863-1792; SPIN: 3634-8816
Anatoly V. Skalny – Dr.Sc. (Med.), Professor,
Head of the Department of Medical Elementology of Medical Institute;
Director of the Centerfor Bioelementology and Human Ecology
E-mail: skalnyy-aa@rudn.ru; ORCID: 0000-0001-5310-3853; SPIN: 9069-0962
Evgeny A. Bezrukov – Dr.Sc. (Med.), Vice-Principal for Innovation and Clinical Activities;
Professor at the Institute of Urology and Human Reproductive Health
SPIN: 2208-2676
Vladimir I. Torshin – Dr.Sc. (Biol.), Professor,
Head of the Normal Physiology Department of Medical Institute
ORCID: 0000-0002-3950-8296; SPIN: 8602-3159
Alexander E. Severin – Dr.Sc. (Med.),
Professor of the Normal Physiology Department of Medical Institute
SPIN: 7297-4092
Conflict of interest
The authors declare no obvious and potential conflicts of interest related to the publication of this article.