No abstract

The present study was done to evaluate the pituitary-testicular activities of rats subjected to chronic nicotine treatment. The testicular key androgenic enzymes activities, plasma and intratesticular testosterone (ITT) concentrations, and plasma concentration of gonadotropin were significantly reduced by nicotine treatment along with the decreased sperm counts and the disruption of spermatogenesis indicated by significant reduction in the number of different generations of germ cells at stage VII of the spermatogenesis cycle with increased sperm head abnormalities. The Western blot and the reverse transcriptase-PCR analysis revealed that the nicotine induced a marked decrease in the expression of testicular steroidogenic acute regulatory (StAR) protein, which helps in the transfer of cholesterol in mitochondria for the testosterone biosynthesis. The increased testicular lipid peroxidation, plasma concentration of corticosterone, with enhanced hydrogen peroxide and hydroxyl radical generations, as well as decreased glutathione level, reduced antioxidant enzymes activities, and mitochondrial membrane potential (Deltapsi(m)) of testis, were noted after nicotine treatment in rats. Human chorionic gonadotropin or taurine supplementation with nicotine prevented the degeneration of germ cells to some extent, restored spermatogenesis moderately with decreased sperm head abnormalities, and enhanced sperm counts, accompanied with increase in plasma and ITT concentrations, testicular StAR gene expression, and key androgenic enzymes activities. Moreover, taurine supplementation to nicotine-treated animals resulted in the diminution of testicular lipid peroxidation, hydrogen peroxide and hydroxyl radical generations, with the elevation in glutathione level as well as different antioxidant enzymes activities and Deltapsi(m) in testis. The results indicated that nicotine caused testicular toxicity by germ cell degeneration, inhibition of StAR gene expression along with androgen production in adult male rats probably by affecting pituitary gonadotropin, and/or modulating the extent of testicular antioxidant status.

The present study focused an chronic intensive exercise-induced oxidative stress that may cause dysfunctions in male reproductive system including steroidogenesis and spermatogenesis.

No abstract

BackgroundCalcium chloride solution is an established injectable sterilant in dogs and other mammals. With cat populations a continuing problem, we sought to explore its first use in cats. Six cats per group were injected with 5%, 10% or 20% calcium chloride dihydrate in saline solution with lignocaine hydrochloride, a local anaesthetic.ResultsAt the 60th day post-injection, cat testes were collected and showed complete testicular necrosis and replacement by fibrous tissue; very low sperm counts; and reduction of serum testosterone by at least 70% in 20% dose. Androgenic enzyme activities and their expressions were also reduced in all the treated groups along with intra-testicular testosterone concentration was also low. Increased testicular lipid peroxidation, with reduced antioxidants and mitochondrial membrane potential, were evident following calcium chloride treatments. However, there were no apparent changes in serum concentrations of cortisol, fasting blood sugar level, blood urea nitrogen, packed cell volume, or total serum protein following calcium chloride injection, suggesting that this method of sterilization is not associated with any general stress response.ConclusionCalcium chloride solution demonstrates potential for androgenesis-eliminating nonsurgical sterilization of male cats in addition to its proven efficacy in dogs and other mammals.

Background: Inorganic arsenic is a major water pollutant and a known human carcinogen that has a suppressive influence on spermatogenesis and androgenesis in male reproductive system. However, the actual molecular events resulting in male reproductive dysfunctions from exposure to arsenic remain unclear. In this context, we evaluated the mode of action of chronic oral exposure of sodium arsenite on hypothalamo-pituitary-testicular activities in mature male albino rats.

No abstract

In the present study, 30 male rats (age 3 mos, Wt 128.6 +/- 3.7 g) were randomly divided into Control group (CG), Experimental group (EG), and Supplemented group (SG), 10 per group. An exercise protocol (3 hrs swimming per day, 5 days a week for 4 weeks) was followed in EG and SG, with no exercise in CG. In SG, alpha-tocopherol succinate was injected sub-cutaneously at a dose of 50 mg x kg(- 1) per body weight per day. After 4 weeks of exercise, significant diminutions (p < 0.05) were noted in somatic indices of testes and accessory sex organs; seminiferous tubuler diameter (STD); testicular (delta (5), 3 beta-hydroxysteroid dehydrogenase delta(5), 3 beta-HSD), 17 beta-hydroxysteroid dehydrogenase (17 beta-HSD) activities; plasma levels of testosterone (T), luteinizing hormone (LH); preleptotine spermatocytes (pLSc), mid-pachytene spermatocytes (mPSc), and Stage 7 spermatids (7 Sd); testicular alpha-tocopherol and glutathione (GSH) content; superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPX), and glutathione-s-transferase (GST) activities in EG when compared to CG. Moreover, a significant elevation (p < 0.05) in malondialdehyde (MDA) was found in testes of EG compared to CG. No significant alteration was noted in body weight among the groups. Co-administration of alpha-tocopherol succinate restored the above parameters. Intensive swimming exercise-induced oxidative stress causes dysfunction in the male reproductive system, which can be protected by alpha-tocopherol succinate.