Effect of vitamin E administration on histopathological changes in rat testes following torsion and detorsion.

INTRODUCTION: Testicular torsion is a medical emergency, especially in male neonates and adolescents. It is a common clinical outcome and a significant urological issue. From the literature, it is evident that the use of antioxidants in the prevention of testicular reperfusion injury following detorsion is conflicting. This study was conducted to investigate the role of vitamin E in testicular reperfusion injury following detorsion. METHODS: Male Wistar albino rats were divided into Groups I, II, III and IV. Only Group IV rats were pre-treated with vitamin E 100 mg/kg body weight for 30 days. Ischaemia was induced manually by rotating the rat testis to 720 degrees clockwise and counter rotating for reperfusion. The testes were fixed in Bouin's fluid and processed for histopathological examination. RESULTS: A significant decrease in the standard tubular diameter and epithelial height was observed in Group III rats compared to those in Groups I and II. However, the seminiferous tubules in Group IV rats showed recovery in the standard tubular diameter and epithelial height when compared with the untreated control groups. CONCLUSION: The results showed that vitamin E, when administered before torsion of the spermatic cord in rats, provided significant protection against acute testicular torsion and detorsion injury.

The reproductive toxicity of the organophosphate pesticide 0, 0-dimethyl 0-4-nitrophenyl phosphorothioate (methyl parathion) in the male rat.

Methyl parathion (MP) is a pesticide widely used to protect crops but also illegally used in many countries for spraying homes and businesses to contain insects. The present study was planned to investigate the effects of MP on the male reproductive organs in the rat. Male Wistar rats (13-14 weeks old) were treated with MP and sacrificed as follows. Experiment 1:0 (water vehicle), 1.75, 3.5 or 7 mg/kg (i.p.) for 5 days and sacrificed on day 14; experiment 2:0, 0.5 or 1 mg/kg (i.p.) for 12 days and sacrificed on day 130; experiment 3: 0, 0.5 or 1 mg/kg (i.p.) for 12 days and sacrificed on day 77; experiment 4: 0, 0.75 or 1.5 mg/kg (i.p.) for 25 days and sacrificed on day 17; experiment 5: 0 or 3.5 mg/kg (p.o.) for 25 days and sacrificed on day 17 after the last exposure. The reproductive organs were removed, weighed and processed for histopathological analysis. Structural changes, for example the morphology of the epithelium and the lumina of the organs, were observed in all animals. Biochemical estimates of acid phosphatase (ACP), cholesterol, total protein, uric acid, and vitamin C were conducted in the epididymes. The weight of the epididymes increased in experiment 2 in a dose-dependent pattern (p < 0.01) and decreased in experiments 4 and 5 (p < 0.01). The weight of the ductus deferens decreased in experiment 3 at 1 mg/kg dose level (p < 0.001) and increased in experiment 5 (p < 0.05). The weight of the seminal vesicle decreased in experiment 3 at both 0.5 mg/kg and 1 mg/kg dose levels (p < 0.001), and increased in experiment 5 (p < 0.01). The weight of the prostate decreased in experiments 4 (in a dose-dependent pattern) and 5 (p < 0.001). ACP levels decreased in experiment 4 (p < 0.001) with a greater effect at 0.5 mg/kg than at 1 mg/kg. In experiment 5 (p < 0.01) cholesterol levels decreased to less than 50% of the control level for this experiment (p < 0.01) and protein levels also decreased (p < 0.01). Vitamin C levels decreased in a dose-dependent pattern in experiments 4 (p < 0.001) and 5 (p < 0.01). There were no effects on uric acid level. Sperm density was decreased in the epididymes of the rats treated and the epithelium of the epididymis and ductus deferens showed cellular necrosis, brush-border disruption and nuclear pyknosis. Nuclei were haloed, except in experiment 2 and the 0.5 mg/kg group of experiment 3. Methyl parathion did not induce significant changes in the structure of the seminal vesicle and prostate, except that epithelial folding was shorter than in the control. In conclusion, MP is a reproductive toxicant in the male rat and causes deterioration in the structural integrity of the reproductive organs and also the biochemical parameters in the epididymis.

Neonatal methyl parathion exposure affects the growth and functions of the male reproductive system in the adult rat.

Methyl parathion (MP) is a well-known organophosphorus pesticide, to which humans are exposed in fruit and vegetables as residues of 0-2 mg/kg, children being at higher risk of exposure. The present study was planned to investigate the effects on the adult male reproductive functions of MP following neonatal exposure. New born male Wistar rat pups were treated orally with either 0 or 0.5 mg/kg MP from postnatal day (PND) 3 to PND 28 and sacrificed on PND 98 for the purpose of examination of the reproductive system. Methyl parathion lowered the body weights from days 10 to 24 (p < 0.01), the weights of the reproductive organs (p < 0.05-0.01), the epididymal sperm count (p < 0.01) and the homogenisation-resistant testicular spermatid head count (p < 0.01) and also decreased acid phosphatase (ACP), cholesterol, uric acid, protein, ascorbic acid, and lactate dehydrogenase (p < 0.01) levels in the testis but only ACP and cholesterol in the epididymis. The levels of abnormal sperm and testosterone in the testis were increased (p < 0.01), whereas the leutinising hormone level and total number of seminiferous tubules decreased in the testes of treated rats (p < 0.01). A few tubules showed exfoliation of epithelium and vacuoles. The incidence of stage XIV tubules and ratios of meiotic figures and elongating spermatids to Sertoli cell nucleoli decreased (p < 0.01; Mann-Whitney U test). The present results indicate that MP acts as an endocrine disruptor and consequently affects the postnatal development and growth of the male reproductive organs in the rat. These findings are important to the general public, as there is a chance of children being exposed to this pesticide.

A broad-spectrum organophosphate pesticide O,O-dimethyl O-4-nitrophenyl phosphorothioate (methyl parathion) adversely affects the structure and function of male accessory reproductive organs in the rat.

Methyl parathion (MP) is an organophosphate pesticide used in agriculture, but also illegally used to spray homes and businesses to control insects. The present study was designed to investigate adverse effects of MP on accessory reproductive organs. Male Wistar rats aged 13-14 weeks were treated and sacrificed as follows. Experiment 1: 0.0 (water vehicle), 1.75, 3.5 or 7mg/kg (i.p.) for 5 days and sacrificed on day 14; experiment 2: 0.0, 0.5 or 1mg/kg (i.p.) for 12 days and sacrificed on day 130; experiment 3: 0.0, 0.5 or 1mg/kg (i.p.) for 12 days and sacrificed on day 77; experiment 4: 0.0, 0.75 or 1.5mg/kg (i.p.) for 25 days and sacrificed on day 17 and experiment 5: 0.0 or 3.5mg/kg (p.o.) for 25 days and sacrificed on day 17, after the last exposure. The accessory reproductive organs were removed, weighed and processed for histopathological analysis. Structural qualitative changes such as epithelial cell morphology and luminal observations were carried out for each organ in all experiments. Epididymis of one side was homogenized and biochemical estimations of acid phosphatase (ACP), cholesterol, total protein, uric acid, and Vitamin C were conducted by calorimetric methods in experiments 4 and 5. In experiment 1 the organ weights did not change; in experiment 2, the epididymal weight increased (P<0.001); in experiment 3, the weights of ductus deferens decreased at 1mg/kg and that of seminal vesicle decreased at both dose-levels (P<0.001). In experiments 4 and 5, weights of epididymis and prostate decreased, whereas in experiment 5, weights of ductus deferens and seminal vesicle increased (P<0.05-0.001). The sperm density was normal in control, moderately decreased in experiment 1 at 3.5 and 7mg/kg; in experiment 2 at 1mg/kg, and in experiment 5 at 3.5mg/kg, and severely decreased in experiment 3 at 1mg/kg and in experiment 4 at both dose-levels. The epithelial necrosis and nuclear pyknosis were seen in experiments 1, 3, 4 and 5, whereas nuclear degeneration was seen in experiment 1 and 4 and germ cells in the lumina of epididymis were seen in experiment 4. The nuclear pyknosis in the ductus deferens was seen in all experiments, except at 1.75mg/kg in experiment 1 and at 0.5mg/kg in experiment 3. Brush border disruption in the ductus deferens was seen in experiments 1 and 4; sperms were seen in the lumen in experiment 1 at 7mg/kg, and in experiments 4 and 5. The vacuoles in the epithelium were seen in experiments 1 and 4 and immature germ cells were seen in the lumen in experiment 4. The ACP and Vitamin C levels decreased in experiment 4 at both dose-levels, and in experiment 5 all biochemical parameters tested found decreased (P<0.01-0.001). The present results indicate that MP affects the structure and function of accessory reproductive organs in the rat.

Effects of methyl parathion (o,o-dimethyl o-4-nitrophenyl phosphorothioate) on rat sperm morphology and sperm count, but not fertility, are associated with decreased ascorbic acid level in the testis.

Methyl parathion (MP; o,o-dimethyl o-4-nitrophenyl phosphorothioate) is an organophosphorous pesticide used world wide to spray agricultural crops. The present study was aimed to investigate the genotoxic and cytotoxic effects on male germ cells and their possible relation with testicular ascorbic acid levels. Adult male Wistar rats (n=5/group) received MP at 0, 0.5, or 1 mg/kg (experiments 1 and 2) for 12 days and 0, 0.75 or 1.5 mg/kg (experiment 3) for 25 days (i.p.) everyday at intervals of 24 h. The epididymal sperm count, sperm abnormalities and testicular ascorbic acid levels (by 2,4-dinitrophenyl hydrazine method) were estimated on days 130, 77 and 17 following the last exposure in experiments 1, 2, and 3, respectively. Virgin untreated female rats were mated with treated males from experiments 2 and 3 for a week effective from day 35 to 41 after the first treatment, and fertility indices were measured after the birth of pups. Sperm count was decreased in experiments 2 and 3 (P<0.01), and in all three experiments, the abnormal sperms increased (P<0.001). Concomitantly, the ascorbic acid levels decreased in the testis (P<0.05-0.001; one-way ANOVA and Bonferroni's post hoc test). The body weights of offspring of treated males did not show significant changes from those of the controls, although there were some decreases observed. MP reduced the lactation index in experiment 2 (P<0.001; Chi-square test). The number of pups/parent along with fertility indices showed some numerical decrease but without any statistical significance. The present findings suggest that MP is a weak genotoxic and cytotoxic agent in the rat exposed to human exposure dose-levels, and that these effects, except the fertility are well correlated with decreased ascorbic acid level in the testis. Furthermore, MP-induced changes in the germ cells do not have any significant effects on F1 generation.