The involvement of hypophyseal-gonadal and hypophyseal-adrenal axes in arsenic-mediated ovarian and uterine toxicity: modulation by hCG.
This study evaluated the involvement of hypophyseal-gonadal and hypophyseal-adrenal axes as a possible mechanism of sodium arsenite toxicity in ovary and uterus by the coadministration of hCG. Subchronic treatment of 0.4 ppm of sodium arsenite/(100 g body weight day) via drinking water for seven estrous cycles significantly suppressed the plasma levels of leutinizing hormone, follicle-stimulating hormone, and estradiol along with sluggish ovarian activities of Delta(5),3beta-hydroxysteroid dehydrogenase and 17beta-hydroxysteroid dehydrogenase followed by a reduction in gonadal tissue peroxidase activities in mature female rats at diestrous phase. Noticeable weight loss of the ovary and uterus along with prolonged diestrous phase and increased deposition of arsenic in the plasma and in these reproductive organs were also demonstrated following the ingestion of arsenic. Follicular atresia and thinning of the uterine luminal diameter were evident after sodium arsenite treatment. Effective protection of gonadal weight loss, suppressed ovarian steroidogenesis, and altered ovarian and uterine peroxidase activities were noticed when 1.0 IU hCG/(100 g body weight day) is given in arsenic-intoxicated rats. Normal estrous cyclicity was restored toward the control level after hCG coadministration, though the elimination of elementary arsenic from the plasma and gonadal tissues was impossible. A significant recovery in the restoration of ovarian and uterine histoarchitecture was prominent after hCG treatment. Adrenal hypertrophy and steroidogenic arrest of the adrenal gland along with altered level of brain monoamines in the midbrain and diencephalons following arsenic intoxication were also ameliorated after hCG coadministration.
Department of Bio-Medical Laboratory Science and Management (UGC Innovative Department), Vidyasagar University, Midnapore 721 102, West Bengal, India. sandipdoc@yahoo.com
Sandip
S
Chattopadhyay
Debidas
D
Ghosh
D000311:Adrenal Glands / Q000187:drug effects / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology*; D000818:Animals; D001151:Arsenic / Q000032:analysis / Q000097:blood / Q000633:toxicity*; D020261:Arsenic Poisoning / Q000503:physiopathology; D018053:Arsenites / Q000008:administration & dosage; D015306:Biogenic Monoamines / Q000378:metabolism; D001923:Brain Chemistry / Q000187:drug effects; D006063:Chorionic Gonadotropin / Q000627:therapeutic use*; D003345:Corticosterone / Q000097:blood; D004031:Diestrus / Q000187:drug effects; D005260:Female; D005496:Follicular Atresia / Q000187:drug effects; D042341:Gonadal Hormones / Q000097:blood / Q000378:metabolism; D009929:Organ Size / Q000187:drug effects; D010053:Ovary / Q000187:drug effects* / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology*; D010544:Peroxidases / Q000378:metabolism; D010913:Pituitary-Adrenal System / Q000187:drug effects / Q000503:physiopathology*; D051381:Rats; D017208:Rats, Wistar; D017670:Sodium Compounds / Q000008:administration & dosage; D014599:Uterus / Q000187:drug effects* / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology; D014874:Water Pollutants, Chemical / Q000633:toxicity
D018053:Arsenites; D015306:Biogenic Monoamines; D006063:Chorionic Gonadotropin; D042341:Gonadal Hormones; D017670:Sodium Compounds; D014874:Water Pollutants, Chemical; C017947:sodium arsenite; D010544:Peroxidases; D001151:Arsenic; D003345:Corticosterone