ABSTRACT
Arsenic-associated human health complications are reported worldwide. Although inorganic arsenic has long been known to be toxic to humans, little is known about its metabolite, dimethylarsinic acid and its toxicity. We investigated the hepatic toxicity of dimethylarsinic acid and its interaction with iron and lipopolysaccharide in drinking water. Rats were given drinking water with dimethylarsinic acid with or without iron for three weeks. Dimethylarsinic acid alone, iron alone, and dimethylarsinic acid-plus-iron treatment did not cause hepatic damage. A single dose of lipopolysaccharide increase hepatic damage in dimethylarsinic acid-puls-iron-treated rats. We hypothesize that exposure to lipopolysaccharide increases hepatic damage in dimethylarsinic-acid-plus-iron-treated rats
ABSTRACT
<p><b>AIM</b>To study the effect and mechanism of gonadotrophin-releasing hormone (GnRH) on murine Leydig cell steroidogenesis.</p><p><b>METHODS</b>Purified murine Leydig cells were treated with GnRH-I and -II agonists, and testosterone production and steroidogenic enzyme expressions were determined.</p><p><b>RESULTS</b>GnRH-I and -II agonists significantly stimulated murine Leydig cell steroidogenesis 60%-80% in a dose- and time-dependent manner (P < 0.05). The mRNA expressions of steroidogenic acute regulatory (StAR) protein, P450scc, 3beta-hydroxysteroid dehydrogenase (HSD), but not 17alpha-hydroxylase or 17beta-HSD, were significantly stimulated by both GnRH agonists with a 1.5- to 3-fold increase (P < 0.05). However, only 3beta-HSD protein expression was induced by both GnRH agonists, with a 1.6- to 2-fold increase (P < 0.05).</p><p><b>CONCLUSION</b>GnRH directly stimulated murine Leydig cell steroidogenesis by activating 3b-HSD enzyme expression.</p>