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Cigarette smoking appears to have adverse effects of male reproductivity. The interplay between zinc and cadmium presumably plays a role in mediating toxic effects of smoking. This work was conducted to study serum and seminal plasma zinc and cadmium level in smokers compared to non-smokers. Seventy males were included: 35 smokers (group I) (smoking ˃20 cigarettes/day with mild smoking index <400) and 35 age-matched non-smokers (group II). Semen analysis was performed according to the WHO laboratory manual 2010. Atomic absorption spectrophotometer was used to detect zinc and cadmium amounts in both blood plasma and semen of any groups. Smoker group showed significantly lower sperm density, motility (P=0.001), and sperm viability (P=0.002) and higher abnormally formed sperms. Seminal zinc level was significantly lower in smokers (P=0.038).There was significant negative correlation between seminal zinc and smoking index and significant positive correlation between seminal zinc levels and sperm motility (P=0.008) and viability percentage (P=0.001). Seminal cadmium level was significantly higher in smoker (P=0.022). Significant positive correlation between seminal cadmium and both age and smoking index (P=0.003) and significant negative correlation between seminal cadmium and sperm density (P=0.005), motility (P=0.047), and viability (P=0.039). Seminal zinc level was negatively correlated to seminal cadmium level (P=0.020). Smoking has deleterious effects on semen quality hence fertility through several toxicants and chemicals. Reduced zinc levels and elevated cadmium levels were evident in smokers which have significant role in the adverse effects on the semen parameters., (© 2021. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.)

Prostate cancer is one of the most common cancers and the second cause of cancer-related deaths among men. Metals are recognized as chemical carcinogens where chronic exposures to such metals are implicated in the development of cancer, including prostate cancer. This in vitro study demonstrates the relative death sensitivity of prostatic (RWPE-1) cells to arsenic (As), cadmium (Cd), and chromium (Cr) as environmental pollutants through its apoptotic effects and the effect of these chemicals on prostate-specific antigen (PSA) gene expression as a marker for their carcinogecity. RWPE-1 cells were divided into three groups that were treated with As, Cd, and Cr in three replicates, at three different concentrations for each metal for 48 h. A control group consisted of untreated RWPE1 cells was used. Apoptosis was assessed using comet assay and caspase 3 gene expression; meanwhile, PSA gene expression was evaluated by semiqualitative real-time PCR (RT-PCR). One of the novel findings of this study is that arsenic and cadmium at low concentrations decreased apoptosis of RWPE-1 cells in a concentration-dependent manner while chromium induced significant concentration-dependent increase in apoptosis. Yet, at the highest concentrations, apoptosis was relatively more induced by all chemicals. Arsenic was the most chemical inhibiting apoptosis in RWPE-1 cells at low concentration. While at the moderate and highest concentrations, cadmium was the most inhibiting chemical of RWPE-1 cells' apoptosis. No distinct differences between treated and untreated cells for PSA gene expression were observed. It can be concluded that As and Cd, at low concentrations, can reduce apoptosis of prostatic cells in a concentration-dependent manner while chromium induced it; however, all metal salts used in this study did not induce PSA gene expression.