Nickel-induced oxidative stress in testis of mice: evidence of DNA damage and genotoxic effects.

摘要: Oxidative stress (OS) mechanisms are speculated to play a significant role in nickel-induced toxic effects and their carcinogenic potency. Although oxidative damage somatic tissues is well demonstrated, evidence of the involvement similar mechanism(s) testicular dysfunction associated genotoxic scarce. Hence, present study aimed investigate OS response testis implications vivo. Initially, toxicity profile nickel chloride was determined adult albino mice (CFT-Swiss) following administration (intraperitoneal) single doses. Subsequently, multiple sublethal doses (1.25, 2.5, 5.0 micromol/100 g body weight per day for 3 days) were used characterize on histoarchitecture, lipid peroxidation (LPO) (homogenates, microsomal or mitochondrial fractions) epididymal sperm, DNA damage, induction apoptosis testis, incidence sperm head abnormalities. short-term induced only minimal LPO response, elicited moderate (15% 30%) increase whole homogenates higher dose-related increases both (20% 50%) fractions (25% 60%). This with as evidenced by increased single-strand breaks (fluorimetric analysis unwinding assay). Further, at doses, demonstrable biochemically. caudal counts all sampling weeks showed no alterations, abnormalities revealed nearly 3- 4-fold percentage abnormal sperms among nickel-treated males during first weeks. Furthermore, mating (2.5 5 sequentially period untreated females resulted male-mediated dominant lethal-type mutations (the frequency dead implantations) weeks, suggesting stage-specific effect postmeiotic germ cells. These findings suggest that compounds may be related enhanced production reactive oxygen species, probably mediated through macromolecules, including DNA.