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Nickel toxicology with reference to male molecular reproductive physiology

Rizvi, Asim, Parveen, Saima, Khan, Saniyya, Naseem, Imrana
Reproductive Biology 2020 v.20 no.1 pp. 3-8
DNA-binding proteins, apoptosis, carcinogenesis, contact dermatitis, epigenetics, genes, humans, male reproductive system, males, metabolism, nickel, oxidation, oxidative stress, pathophysiology, protamines, reactive oxygen species, spermatozoa, toxicity, toxicology, zinc
The toxicity of metals is a known phenomenon. Nickel toxicity is very common since nickel is used extensively both industrially and in items of personal use such as utensils and jewellery. Here we discuss human exposure to nickel and its toxicity in the light of the available scientific evidence to understand its underlying pathophysiology. The ability of Ni⁺² to get oxidized to Ni⁺³ renders it’s potential of generating reactive oxygen species (ROS) in the system leading to oxidative stress. Carcinogenesis, apoptosis induction, contact dermatitis, epigenetic changes, and alteration in gene regulation are a result of overexposure of nickel. Our focus is on how nickel affects the male reproductive physiology. Nickel primarily drives ROS mediated perturbations in the male reproductive system. It influences zinc metabolism, which is critical for sperm stability and affects the structure of DNA binding proteins, including protamines, thereby affecting sperm function.