Department of Bio-Medical Laboratory Science and Management (UGC Innovative Department), Vidyasagar University, Midnapore 721 102, West Bengal, India.
J Biochem Mol Toxicol. 2010 Jan-Feb;24(1):29-41. doi: 10.1002/jbt.20309.
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.
这项研究通过给予 hCG，评估了脑垂体-性腺和脑垂体-肾上腺轴作为亚砷酸钠对卵巢和子宫毒性的可能机制。通过饮用水给予 0.4ppm 的亚砷酸钠（100g 体重/天）进行为期七个发情周期的亚慢性处理，显著抑制了发情间期成熟雌性大鼠血浆黄体生成素、卵泡刺激素和雌二醇水平，以及卵巢 Delta(5)、3β-羟甾脱氢酶和 17β-羟甾脱氢酶活性的降低，随后性腺组织过氧化物酶活性也降低。在摄入砷后，还观察到卵巢和子宫明显减重、发情间期延长以及血浆和这些生殖器官中砷的沉积增加。卵泡闭锁和子宫腔直径变薄在亚砷酸钠处理后是明显的。当在砷中毒大鼠中给予 1.0IU hCG（100g 体重/天）时，观察到性腺重量减轻、卵巢类固醇生成抑制和卵巢和子宫过氧化物酶活性改变得到有效保护。虽然从血浆和性腺组织中消除初级砷是不可能的，但 hCG 共给后，发情周期恢复到对照水平。hCG 处理后，卵巢和子宫组织形态结构的恢复明显恢复。砷中毒后，中脑和间脑的脑单胺水平也会导致肾上腺肥大和肾上腺类固醇生成停滞，hCG 共给后也得到改善。
