Introduction: Arsenic is a potent environmental toxin associated with male infertility. Taurine (TAU) has been demonstrated to regulate oxidative stress biomarkers and improve mitochondrial function. Materials and Methods: It evaluated the hypothesis that TAU could recover spermatogenesis dysfunction in an arsenic-treated rat model. Then, 24 adult male rats were challenged as follows (n=6/group) for 35 consecutive days: control (distilled water; gavage); 3 mg/l/day sodium arsenite; TAU (1000 mg/kg; 14) during arsenic exposure; and TAU during the study period. 24 h after the last treatment, animals were euthanized, serum samples were processed for assessing sex hormone levels, and testes were processed for weight, oxidative stress indices, histopathology, and RNA extraction for expression levels of autophagic marker genes. Results: Arsenic causes defective pathologic effects, and upregulates autophagic marker gene expression and production of free radicals. TAU exposure notably ameliorated the autophagy dysregulation through downregulation of the autophagic genes by inhibition of oxidative changes. Conclusion: This study presents a novel scientific approach to arsenic spermatogenesis dysfunction, attributed to TAU’s antioxidant activity.

Objective(s): Varenicline is a selective partial agonist for the nicotinic acetylcholine receptor a4b2 subtype, which is widely used to treat smoking addiction. However, there is still no data about its potential toxic effects on tissues. In this study, we aimed to determine the varenicline-induced toxicity on reproductive and renal tissues in rats. Materials and Methods: Rats were randomly divided into two groups: control (n=10) and varenicline (n=24). Then, rats in each group were sub-divided equally as acute and chronic groups. The control rats were orally given distilled water only. Varenicline was administrated orally as follows: 1st– 3rd days 9 μ g/kg/day, 4th– 7th days 9 μ g/kg twice daily, and 8th– 90th days 18 μ g/kg twice daily. The rats of acute and chronic groups were sacrificed on the 45th and 90th days, respectively. Some tissue markers related to oxidative stress were measured, and sperm characteristics were observed. Results: In the acute group, varenicline led to a significant decrease in SOD activities in both kidney and testis tissues. In the chronic group, varenicline significantly increased MDA and MPO production, and reduced CAT and GPx levels in the kidneys and testes. Also, SOD and GSH levels significantly decreased in the testes. Moreover, sperm characteristics were negatively affected; histopathological deformation was observed in the testes and kidneys in all groups. Conclusion: This study showed that varenicline could detrimentally affect the kidneys and testes in both acute and chronic term usage. Further studies will provide more insights into the molecular dynamics of this damage.