Effects of dietary magnesium on testicular histology, steroidogenesis, spermatogenesis and oxidative stress markers in adult rats.

The available information on the effect of excess dietary magnesium on male reproduction is inadequate, though consumption of hard water rich in magnesium salt is not uncommon in many geographical areas. The present study has thus been undertaken to evaluate the morphological as well as cytological and functional changes in testis of magnesium administered sexually mature male Wistar rats. Significant increase in the activities of androgenic enzymes viz. delta(5)3beta-hydroxysteroid dehydrogenase and 17beta-hydroxysteroid dehydrogenase with concomitant increase in serum testosterone level, followed by progressive development in cytoarchitechture of genital organs, without any significant alteration in quantitative spermatogenesis were observed. The results were more marked in the groups treated for longer duration. The results further suggests that the changes that occurred after excessive magnesium in testis were not for the enhanced adrenocortical activities or for the generation of oxidative stress in reproductive organs, but for the direct action of excess magnesium on male gonads. Magnesium supplementation thus has an apparent beneficial effect on male gonadal system.

Excessive dietary calcium in the disruption of structural and functional status of adult male reproductive system in rat with possible mechanism.

Calcium is essential for functioning of different systems including male reproduction. However, it has also been reported as chemo-castrative agent. The study has been undertaken to elucidate the effect of excessive dietary calcium on male reproductive system in animals with possible action. Adult male healthy rats fed CaCl(2) at different doses (0.5, 1.0 and 1.5 g%) in diet for 13 and 26 days to investigate reproductive parameters as well as the markers of oxidative stress. Significant alteration was found (P < 0.05) in testicular and accessory sex organs weight, epididymal sperm count, testicular steroidogenic enzyme (Δ(5) 3ß-HSD and 17ß-HSD) activities, serum testosterone, LH, FSH, LPO, activities of antioxidant enzymes, testicular histoarchitecture along with adrenal Δ(5) 3ß-HSD activity with corticosterone level in dose- and time-dependent manner. Overall observations suggest that excessive dietary calcium enhances the generation of free-radicals resulting in structural and functional disruption of male reproduction.

Effect of green tea (Camellia sinensis L.) extract on morphological and functional changes in adult male gonads of albino rats.

Green tea, prepared from the steamed and dried leaves of the shrub Camellia sinensis, is known for its antioxidant and anti-carcinogenic effects. However, its effects on male gonadal functions have not been explored adequately and the present investigation has been undertaken to evaluate the effect of green tea extract on gonads of adult male albino rats. Results of in vivo studies showed that green tea extract (GTE) at mild (1.25 g%, identical to 5 cups of tea/day), moderate (2.5 g%, identical to 10 cups of tea/day) and high (5.0 g%, identical to 20 cups of tea/day) doses, for a period of 26 days, altered morphology and histology of testis and accessory sex organs. A significant dose-dependent decrease in the sperm counts, inhibited activities of testicular delta(5)3beta-and 17beta-hydroxysteroid dehydrogenase (delta5-3beta3-HSD and 17beta3-HSD respectively) and decreased serum testosterone level were noticed. Significant increase in serum LH level was observed after moderate and high doses; serum FSH level also increased but not significantly. Histopathological examination showed inhibition of spermatogenesis evidenced by preferential loss of matured and elongated spermatids. Results of this study showed that GTE at relatively high dose may cause impairment of both the morphological and normal functional status of testis in rodents and thus its consumption at relatively high doses raises concern on male reproductive function in spite of its other beneficial effects.

Protection against vanadium-induced testicular toxicity by testosterone propionate in rats.

Vanadium is a well recognized industrial hazard known to adversely affect male reproductive functions. The intricate mechanistic aspects of this metal and the role of oxidative stress in the deterioration of testicular functions are investigated in the current study. The experiment also focused on the effects of testosterone propionate in testicular and sperm functions in the rat intoxicated with vanadate. Vanadium exposure resulted in a more prominent spermatogenic arrest and consistently abolished the conversion of round to mature spermatids along with decreased epididymal sperm number and increased percentage of abnormal sperm. This is followed by a precipitous decline in the level of serum testosterone and gonadotropins and consequently the testicular steroidogenic and antioxidant enzymes were inhibited. Vanadium induces degeneration in the genital organs of rats and exhibits high indices of lipid oxidative damage. In response to exogenous testosterone propionate (TP) administration, spermatogonial cell populations remained suppressed, while the spermatogenesis was restored quantitatively. In contrast, the hormone treatment had no effect on the dramatically decreased serum FSH level after vanadate treatment. Moreover, TP could ameliorate the toxicity, as indicated by decreased testicular lipid peroxidation with marginal but significant increase in the activities of all the measured enzymes following vanadate-treatment. Taken together all these studies establish that vanadium is a testicular toxicant that perturbs the male reproductive system adversely. However, hormone replacement therapy by testosterone propionate may provide partial protection. The results suggest the feasibility of using endocrine regimens to impede deleterious effects of vanadium on the male reproductive system.

Vitamin E-supplementation protect chromium (VI)-induced spermatogenic and steroidogenic disorders in testicular tissues of rats.

Excess chromium (Cr) exposure is associated with various pathological conditions including reproductive dysfunction. Generation of oxidative stress is one of the plausible mechanisms behind Cr induced cellular deteriorations. The efficacy of vitamin E to combat Cr induced oxidative damage in adult rat testis has investigated in the current study. Adult male rats exposed to hexavalent Cr (intraperitoneal injection with 0.4 mg K(2)Cr(2)O(7)/ kg bw/day) for 26 days resulted in decreased accessory sex organs weight compared to controls. Development of oxidative stress in testis was evidenced by increased lipid peroxidation along with decreased superoxide dismutase (SOD) and catalase activities than control animals. Marked reduction in the activities of testicular steroidogenic enzymes; Delta(5)3beta-hydroxysteroid dehydrogenase (HSD), 17beta-HSD, serum testosterone and Leutinizing Hormone (LH) levels were observed. However significant increase in serum Follicle Stimulating Hormone (FSH) level was observed with Cr treated group. Histological evaluation of testis revealed degeneration of stage VII spermatogenic cycle along with decrease in epithelial cell height in epididymis and seminiferous tubules; number of different germ cells per seminiferous tubule and seminiferous tubular diameter reduced after Cr exposure. Simultaneous oral supplementation of vitamin E (50mg/kg bw/day) in Cr exposed rats showed less oxidative damage and restored the otherwise altered testicular activities. Epididymal sperm number was also restored in vitamin E-supplemented group than Cr induced rats. This study implicates vitamin E as a possible protective agent against Cr induced spermatogenic and steroidogenic alteration.

Chromium induced testicular impairment in relation to adrenocortical activities in adult albino rats.

The present study investigates the testicular and adrenocortical activities under different doses and durations of chromium (Cr) exposure and their interactions. Mature male Sprague Dawley rats were injected daily with three different doses (0.2, 0.4, and 0.6 mg/kg bw) of Cr salt (K(2)Cr(2)O(7)) intraperitonealy for 13 and 26 days, respectively. The medium (0.4 mg/kg bw/day) and higher dose (0.6 mg/kg bw/day) of Cr significantly (p<0.05) decrease accessory sex organs weight, testicular Delta(5)3beta-hydroxysteroid dehydrogenase (HSD) and 17beta-HSD activities, epididymal sperm count, effective spermatid degeneration, serum testosterone, LH level, testicular catalase and superoxide dismutase (SOD) activities while testicular lipid peroxidation, serum FSH, corticosterone level, adrenal weight and adrenal Delta(5)3beta-HSD activity increased significantly than that of control and lower dose (0.2 mg/kg bw/day) Cr exposed animals. Testicular histoarchitechture shows deterioration after critical dose (0.4 mg/kg bw/day) and duration (26 days) of Cr exposure. Cr induced alterations on testicular and adrenocortical activities are dose and duration dependent. Adrecortical hyperactivity accompanied by testicular oxidative stress might have a crucial role for Cr induced male reproductive impairment.

Amelioration of vanadium-induced testicular toxicity and adrenocortical hyperactivity by vitamin E acetate in rats.

Vanadium toxicity is a challenging problem to the health professionals and a cutting-edge medical problem. Vanadium has been recognized as industrial hazards that adversely affect human and animal reproductive health. Since testicular function is exquisitely susceptible to reactive-oxygen species, the present study elucidates the possible involvement of oxidative stress in vanadium-induced testicular toxicity and the prophylactic effects of vitamin E acetate against such adverse effects of vanadium. The study also characterizes the effects of vanadium on rat adrenal steroidogenesis and determines the underlying mechanisms of testicular and adrenal interactions in response to vanadium exposure. Significantly reduced sperm count associated with decreased serum testosterone and gonadotropins level in the vanadium-injected group of rats compared to control substantially proves the ongoing damaging effects of vanadium-induced ROS on developing germ cells. This is in turn reflected in the appreciable increase in testicular lipid peroxidation level and decline in the activities of steroidogenic and antioxidant enzymes. However, oral administration of vitamin E acetate could protect testes from the toxic effects of vanadium. Vanadium also results in adrenocortical hyperactivity, as evidenced by the elevated secretion of glucocorticoids, adrenal gland hypertrophy and increased activity of adrenal Delta(5)3beta-HSD. However, reversibility of these alterations in adrenocortical activities was vividly reflected after vitamin E acetate supplementation. All these studies reveal that oxidative stress is the major mechanism of health deterioration and that vanadium can act as a stressor metal causing chronic stress effects through excitation of hypothalamo-pituitary-adrenal axis. However antioxidant support by vitamin E acetate may provide significant protection.

Effects of vanadate on male rat reproductive tract histology, oxidative stress markers and androgenic enzyme activities.

Vanadium has been recognized as industrial hazards that adversely affect male reproductive systems of humans and animals. However, less information is available concerning the underlying mechanism in the pathogenesis of male reproductive dysfunction. The present study investigated the possible involvement of oxidative stress to induce oxidative deterioration of testicular functions in adult rats. The results of in vitro and in vivo studies demonstrate that vanadium treatment resulted in a significant dose- and time-dependent increase in the testicular lipid peroxidation, marked inhibition in the level of superoxide dismutase and catalase activities, decreased sperm counts, and substantially inhibited the activities of Delta(5)3beta- and 17beta-hydroxysteroid dehydrogenase as well as serum testosterone level. Histopathological examination revealed inhibition of spermatogenesis and the preferential loss of maturing and elongated spermatids along with increased percent of abnormal sperm. Taken together, the results suggest that an increase in free radical formation relative to loss of antioxidant defense system during vanadium exposure may render testis more susceptible to oxidative damage leading to their functional inactivation. Thus the toxic effects of vanadium are cumulative and that vanadium produced damages in testes are dose- and time-dependent.

Vanadium-induced testicular toxicity and its prevention by oral supplementation of zinc sulphate.

ABSTRACT Transition metal vanadium has been shown to modulate the cellular redox potential and catalyze the generation of reactive oxygen intermediates. Since free radical production and lipid peroxidation are potentially important mediators in testicular physiology and pathophysiology, the present study was conducted to elucidate the vanadium-induced oxidative damages in rat testis and the ameliorative role of zinc sulphate against such adverse effects of vanadium. Adult male rats were dosed for 26 days with daily intraperitoneal injection of 0.4 mg V/kg body weight as sodium metavanadate. One group of rats was treated with zinc sulphate orally simultaneously with vanadium for 26 days, while the other group was treated with zinc sulphate alone. Changes in testicular and accessory sex organ weight, different varieties of germ cells at stage VII of spermatogenic cycle, epididymal sperm count, and enzymatic (Delta(5)3beta- HSD, 17beta- HSD, SOD, catalase), lipid peroxidation, and hormonal milieu were monitored. Vanadium treatment resulted in a significant increase in the testicular lipid peroxidation and caused a marked inhibition in the activities of antioxidant and steroidogenic enzymes. Histopathological examination revealed inhibition of spermatogenesis and the preferential loss of maturing and elongated spermatids. However, coadministration of zinc sulphate to vanadium-treated animals resulted in normalizing these parameters appreciably, emphasizing the therapeutic potentials of zinc. Taken together, the results suggest that an increase in free radical formation relative to loss of the antioxidant defense system during vanadium exposure may render testis more susceptible to oxidative damage, leading to their functional inactivation. However, zinc sulphate supplementation can be an effective antidote in the treatment of vanadium poisoning.

Effect of curcumin on chromium-induced oxidative damage in male reproductive system.

Hexavalent chromium, an environmental contaminant, undergoes redox cycling with generation of free radicals inside the biological system. Curcumin, the yellow bioactive component of turmeric has established its antioxidant activities. The present study evaluates possible ameliorating effects of curcumin on potassium dichromate (K(2)Cr(2)O(7)) (hexavalent chromium) induced reproductive toxicity in adult male Sprague-Dawley rats. Three experimental groups, each consisting of eight rats, were treated with 0.4mg K(2)Cr(2)O(7)/kg bw/day, 0.4mg K(2)Cr(2)O(7)/kg bw/day+20mg curcumin/kg bw on every alternate day and 20mg curcumin/kg bw on every alternate day, respectively, for 26 days. Altered testicular histology, reduced sperm count, low testosterone level, decreased accessory sex organs weight, enhanced lipid peroxidation along with reduced SOD and catalase activities were observed following K(2)Cr(2)O(7) exposure while curcumin supplementation along with K(2)Cr(2)O(7) exposure had shown to prevent the altered parameters. The results thus suggest that curcumin may have a protective role against chromium(VI) induced oxidative damage in male reproductive system.

Effect of gold on stimulation of reproductive function in immature female albino rats.

Significant increase in ovarian and uterine weight and stimulation of ovarian delta5-3beta-hydroxysteroid dehydrogenase (delta5-3beta-HSD) activity and elevation of serum estradiol level were observed following gold chloride (0.2 mg/kg body weight/day), s.c. administration in immature female albino rats. Moreover, normal cyclic changes of estrus were found in vaginal smears of these rats whereas the rats of other groups showed diestrus phase throughout the period of experiment. Histological study of ovary also showed Graafian follicle with ovum in rats treated with 0.2 mg/kg/day of gold proving stimulation of reproductive function, which was not found in the ovarian histological study of other groups including controls. Thus, the results suggest a significant stimulatory effect of gold chloride on female reproductive activity in immature rats. Further, since the above-mentioned changes were evident at a specific dose of gold chloride, the data may have some clinical implications on stimulation and enhancement of fertility in immature female rats.

Hormonal contraceptive like effect of estrogen in milk protein-fed male rats.

Adult male rats received daily injections (sc) of estradiol-17 beta (50 microg/100 g body wt per day) for 7 days. When they were sacrificed 14 days after the last injection, serum levels of gonadotropins and testosterone and weights of accessory sex organs were decreased significantly, testicular 17-hydroxysteroid dehydroganase activity was suppressed and spermatogenesis was inhibited in 5.0% casein-fed estrogen-treated rats. Feeding of 20.0% casein diet to estrogen-treated rats resulted in increased serum concentration of gonadotropins and testosterone. LH and testosterone appeared to be normal in 20.0% casein-fed estrogen-treated rats while serum FSH levels remained subnormal. The estrogen-treated rats fed on 20.0% casein diet showed decreased spermatogenesis in comparison with control rats fed on 20.0% casein diet. Together, these results indicate that high casein diet stimulates synthesis of testicular testosterone and increases serum LH levels more than FSH in estrogen-treated rats. It is concluded that estrogen in the presence of high milk protein diet may be considered to be a suitable steroid hormone in the development of a male contraceptive.

Influence of moonlight on the birth of male and female babies.

Effects of full moon and no moon on the birth of male and female offsprings were studied in Indian Couples of the age group 20 to 40 years. It was observed that 42 wives who were conceived within 24 hours of ovulation at full moon gave birth of 40 male and 2 female babies. On the other hand 40 women conceived on the day of ovulation 3 days prior to full moon gave birth of 13 male and 27 female babies. But only 5 women conceived on no moon, all of them gave birth of female babies. It was also observed that vaginal pH of the ovulated women during full moon was alkaline (pH 8.7 +/- 0.4) while pH was weak acidic in women ovulated 3 days prior to full moon and no moon (pH 6.4 +/- 0.5; 6.2 +/- 0.5). The basal body temperature (BBT) was increased 0.7 degrees F to 1.3 degrees F during the ovulation period when compared with women during the absence of ovulation. But there is an increase in temperature 0.5 degrees F more in women ovulated in full moon than no moon. Together, these results indicate that alkaline vaginal fluid medium and more rise of BBT during full moon favour conception of male [corrected] babies. This method gives the couple more chance of having male child if conception occurs in the day of ovulation in full moon and having female child if conception occurs in no moon.

Effect of sodium arsenite on spermatogenesis, plasma gonadotrophins and testosterone in rats.

AIM: To investigate the effect of arsenic on spermatogenesis. METHODS: Mature (4 months old) Wistar rats were intraperitoneally administered sodium arsenite at doses of 4, 5 or 6 mg.kg(-1).day(-1) for 26 days. Different varieties of germ cells at stage VII seminiferous epithelium cycle, namely, type A spermatogonia (ASg), preleptotene spermatocytes (pLSc), midpachytene spermatocytes (mPSc) and step 7 spermatids (7Sd) were quantitatively evaluated, along with radioimmunoassay of plasma follicle-stimulating hormone (FSH), luteinizing hormone (LH), testosterone and assessment of the epididymal sperm count. RESULTS: In the 5 and 6 mg/kg groups, there were significant dose-dependent decreases in the accessory sex organ weights, epididymal sperm count and plasma concentrations of LH, FSH and testosterone with massive degeneration of all the germ cells at stage VII. The changes were insignificant in the 4 mg/kg group. CONCLUSION: Arsenite has a suppressive influence on spermatogenesis and gonadotrophin and testosterone release in rats.

Effect of copper chloride on adrenocortical activities in adult and immature male rats.

Although copper is an important biological trace element required for normal metabolism, occupational exposure to copper in different industrial workers may result in abnormal rise in plasma copper level which can bring about adverse effects. Intraperitoneal injection of copper chloride at the dose of 2000 µg/kg per day and higher doses for 26 days resulted in significant rise in adrenal weight, adrenal Δ(5)-3ß hydroxysteroid dehydrogenase (HSD) activity and serum corticosterone level in both adult and immature male rats, while 1000 µg/kg per day dose for 26 days duration did not significantly alter the adrenocortical activities and adrenal weight in adult rats. On the contrary, the latter lower dose caused a significant decrease in adrenal Δ(5) 3ß HSD activity and serum corticosterone level in immature male rats.