ToxSci Advance Access published online on July 25, 2003
Toxicological Sciences, doi:10.1093/toxsci/kfg194
Toxicological Sciences © Society of Toxicology 2003; all rights reserved
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1 Reproductive Endocrinology and Family Welfare Research Unit, Dept of Human Physiology with Community Health, Vidyasagar University, Midnapore-721 102, West Bengal, India
* To whom correspondence should be addressed. E-mail: debidas_ghosh{at}yahoo.co.in.
Subchronic treatment of mature female Wistar strain albino rats in diestrous phase with sodium arsenite at a dose of 0.4 ppm/100 g body weight/rat/day via drinking water for period of 28 days (7 estrous cycles) caused a significant reduction in plasma levels of LH, FSH and estradiol along with a significant decrease in ovarian activities of delta five, three beta-hydroxysteroid dehydrogenase (
© 2003 Society of Toxicology
Reproductive and Developmental Toxicology
Effect of Dietary Co-Administration of Sodium Selenite on Sodium Arsenite Induced Ovarian and Uterine Disorders in Mature Albino Rats
Abstract 
5,3
-HSD), seventeen beta-hydroxysteroid dehydrogenase (17-HSD) followed by a reduction in ovarian and uterine peroxidase activities. A significant weight loss of ovary and uterus was also observed after this treatment along with prolonged diestrous phase and high accumulation of arsenic in plasma and these organs. Moreover, sodium arsenite was also responsible for ovarian follicular and uterine cell degeneration characterized by a high number of regressing follicles and reduction in uterine luminal diameter respectively in comparison with control. Dietary supplementation of sodium selenite at the dose of 0.6 mg/100 g body weight/rat/day for a period of 28 days along with arsenic treatment minimized the gonadal weight loss significantly and increased the activities of ovarian steroidogenic enzymes as well as ovarian and uterine peroxidase at control level. Selenium was also able to increase the plasma levels of LH, FSH and estradiol towards control level. Vaginal smear showed normal estrous cyclicity in sodium selenite supplemented arsenic-treated rats along with lower arsenic levels in plasma and gonadal tissue in comparison with arsenic-only treated rats. Histological sections of ovary and uterine tissue in control and experimental group confirmed that sodium selenite supplementation was able to prevent arsenic-induced histopathological changes in the ovary and uterus. Plasma levels of norepinephrine and dopamine in midbrain and diencephalon decreased significantly whereas serotonin level was increased significantly after 28 days of sodium arsenite treatment. All these parameters were in most cases unchanged from control level when sodium selenite was co-administered with sodium arsenite. Arsenic intoxication was also associated with increased liver weight and elevation in the activities of hepatic and renal acid phosphatase, alkaline phosphatase and transaminases, but selenium co-administration was not able to change these toxic effects of arsenic. The results of our experiments indicate the significant protective action of sodium selenite on arsenic-induced toxicity in the female reproductive system, while there was no significant protective effect of selenium on arsenic-induced toxicity in other organs.
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