acid-phosphatase and sodium-arsenite

Toxicity of arsenic was investigated in the gill of Lamellidens marginalis by exposing the animals to sublethal concentrations of sodium arsenite for a maximum period of 30 days in controlled laboratory conditions. Arsenite exposure inhibited the activities of acid phosphatase (ACP), alkaline phosphatase (ALP), glutamate oxaloacetate transaminase (GOT), glutamate pyruvate transaminase (GPT) and acetylcholinesterase (AChE) in a dose and time dependent manner. Depletion in cytotoxic molecule like nitric oxide (NO) and suppression of phenoloxidase (PO) activity suggests an immune compromise in the animal. Inhibition in the activities of glutathione-s-transferase (GST) and catalase (CAT) in the species indicate impairment of its vital detoxification process and elevated oxidative stress respectively. Histopathology of the gill indicates arsenite induced damage of the organ leading to its possible dysfunction. The toxic exposure ravaged the structure and impaired the functions of the gill of the animal which might restrict its proper gaseous exchange, filter feeding and elicitation of immune responses against pathogens.

Topics: Acetylcholinesterase; Acid Phosphatase; Alkaline Phosphatase; Animals; Arsenites; Aspartate Aminotransferase, Mitochondrial; Bivalvia; Catalase; Gills; Glutathione Transferase; India; Monophenol Monooxygenase; Nitric Oxide; Oxidative Stress; Sodium Compounds; Water Pollutants, Chemical

Inorganic arsenic is a major water pollutant and a known human carcinogen that has a suppressive influence on spermatogenesis and androgenesis in male reproductive system. However, the actual molecular events resulting in male reproductive dysfunctions from exposure to arsenic remain unclear. In this context, we evaluated the mode of action of chronic oral exposure of sodium arsenite on hypothalamo-pituitary- testicular activities in mature male albino rats.. The effect of chronic oral exposure to sodium arsenite (5 mg/kg body weight/day) via drinking water without or with hCG (5 I.U./kg body weight/day) and oestradiol (25 micrograms oestradiol 3-benzoate suspended in 0.25 ml olive oil/rat/day) co-treatments for 6 days a week for 4 weeks (about the duration of two spermatogenic cycle) was evaluated in adult male rats. Changes in paired testicular weights, quantitative study of different varieties of germ cells at stage VII of spermatogenic cycle, epididymal sperm count, circulatory concentrations of hormones (LH, FSH, testosterone and corticosterone), testicular activities of delta 5, 3beta-hydroxysteroid dehydrogenase (delta 5, 3beta-HSD), 17 beta-hydroxysteroid dehydrogenase (17 beta-HSD), sorbitol dehydrogenase (SDH), acid phosphatase (ACP), alkaline phosphatase (ALP), and lactate dehydrogenase (LDH), as well as the levels of biogenic amines (dopamine, noradrenaline and 5-hydroxytryptamine (5-HT)) in the hypothalamus and pituitary were monitored in this study. Hormones were assayed by radioimmuno- assay or enzyme- linked immunosorbent assay and the enzymes were estimated after spectrophotometry as well as the biogenic amines by HPLC electrochemistry.. Sodium arsenite treatment resulted in: decreased paired testicular weights; epididymal sperm count; plasma LH, FSH, testosterone and testicular testosterone concentrations; and increased plasma concentration of corticosterone. Testicular enzymes such as delta 5, 3 beta-HSD, 17 beta-HSD, and sorbitol dehydrogenase (SDH) were significantly decreased, but those of acid phosphatase (ACP), alkaline phosphatase (ALP), and lactate dehydrogenase (LDH) were significantly increased. A decrease in dopamine or an increase in noradrenaline and 5-HT in hypothalamus and pituitary were also noted after arsenic exposure. Histological evaluation revealed extensive degeneration of different varieties of germ cells at stage VII of spermatogenic cycle in arsenic exposed rats. Administration of human chorionic gonadotrophin (hCG) along with sodium arsenite partially prevented the degeneration of germ cells and enhanced paired testicular weights, epididymal sperm count, plasma and intratesticular testosterone concentrations, activities of delta 5, 3beta-HSD, 17 beta-HSD and sorbitol dehydrogenase along with diminution in the activities of ACP, ALP and LDH. Since many of the observed arsenic effects could be enhanced by oestradiol, it is suggested that arsenic might somehow acts through an estrogenic mode of action.. The results indicate that arsenic causes testicular toxicity by germ cell degeneration and inhibits androgen production in adult male rats probably by affecting pituitary gonadotrophins. Estradiol treatment has been associated with similar effects on pituitary testicular axis supporting the hypothesis that arsenite might somehow act through an estrogenic mode of action.

Topics: 17-Hydroxysteroid Dehydrogenases; 3-Hydroxysteroid Dehydrogenases; Acid Phosphatase; Alkaline Phosphatase; Animals; Arsenites; Corticosterone; Dopamine; Estradiol; Follicle Stimulating Hormone; Hypothalamo-Hypophyseal System; L-Iditol 2-Dehydrogenase; L-Lactate Dehydrogenase; Luteinizing Hormone; Male; Norepinephrine; Rats; Rats, Sprague-Dawley; Serotonin; Sodium Compounds; Sperm Count; Spermatogenesis; Testis; Testosterone

Long-term exposure to sodium arsenite (AsO(2)) promotes the development of various cancers. Paradoxically, arsenic also induces pro-myelomonocytic leukemia cell differentiation, and at higher concentrations, apoptosis. The present study investigated the effects of AsO(2) on preosteoclasts. When treated with 2.5-5microM AsO(2), RAW264.7 cells underwent osteoclast differentiation as evidenced by an increase in the number of multinucleate cells expressing tartrate resistant acid phosphatase (TRAP). The appearance of these phenotypic markers was preceded by a low level increase in extracellular production of H(2)O(2) and was prevented by the addition of catalase (4.5microg/ml), an enzyme that removes H(2)O(2). Only at high concentrations (10-25microM) of AsO(2) was a significant loss of cell viability and a high level increase in H(2)O(2) production (1.5microM) observed. Apoptosis was blocked by pretreatment with diphenylene iodonium chloride (2microM), a NAD(P)H-flavoprotein inhibitor, suggesting the involvement of NADPH-oxidase. The data show that AsO(2), dose-dependently, stimulates increasing amounts of H(2)O(2) production. Moreover, at concentrations found in tissues of individuals exposed to geochemical AsO(2), osteoclasts underwent an H(2)O(2)-dependent differentiation. Therefore, chronic exposure to low-level amounts of AsO(2) could result in increased bone resorption and contribute to bone related pathologies.

Topics: Acid Phosphatase; Animals; Apoptosis; Arsenites; Caspase 3; Caspases; Cell Differentiation; Cell Line; Cell Survival; Hydrogen Peroxide; In Situ Nick-End Labeling; Isoenzymes; Mice; Osteoclasts; Sodium Compounds; Tartrate-Resistant Acid Phosphatase