Nikolic J, Stojanovic I, Pavlovic R, Sokolovic D, Bjelakovic G, Beninati S
Department of Biochemistry, School of Medicine, University of Nis, Nis, Serbia and Montenegro.
Amino Acids. 2007 Jan;32(1):127-31. doi: 10.1007/s00726-006-0309-y. Epub 2006 May 15.
The existing interrelation in metabolic pathways of L-arginine to polyamines, nitric oxide (NO) and urea synthesis could be affected in sepsis, inflammation, intoxication and other conditions. The role of polyamines and NO in the toxic effect of mercury chloride on rat liver function was studied. Administration of mercury chloride for 24 h led to significantly elevated plasma activities of Alanine transaminase (ALT) and Aspartate transaminase (AST). Malondyaldehyde (MDA) levels were unaffected (p > 0.05) and arginase activity was significantly decreased (p < 0.05) while nitrate/nitrite production was significantly elevated (p < 0.001) in liver tissue. Polyamine oxidase (PAO) and diamine oxidase (DAO) activities, enzymes involved in catabolism of polyamines, were decreased. L-arginine supplementation to intoxicated rats potentiated the effect of mercury chloride on NO production and it was ineffective on arginase activity. Results obtained in this study show that mercury chloride-induced toxicity leads to abnormally high levels of ALT and AST that may indicate liver damage with the involvement of polyamine catabolic enzymes and NO.
L-精氨酸代谢途径与多胺、一氧化氮（NO）及尿素合成之间的现有相互关系，在脓毒症、炎症、中毒及其他情况下可能会受到影响。本研究探讨了多胺和NO在氯化汞对大鼠肝功能毒性作用中的角色。给予大鼠氯化汞24小时后，血浆丙氨酸转氨酶（ALT）和天冬氨酸转氨酶（AST）活性显著升高。肝组织中丙二醛（MDA）水平未受影响（p>0.05），精氨酸酶活性显著降低（p<0.05），而硝酸盐/亚硝酸盐生成显著升高（p<0.001）。参与多胺分解代谢的多胺氧化酶（PAO）和二胺氧化酶（DAO）活性降低。给中毒大鼠补充L-精氨酸增强了氯化汞对NO生成的作用，而对精氨酸酶活性无影响。本研究结果表明，氯化汞诱导的毒性导致ALT和AST异常升高，这可能表明肝脏损伤与多胺分解代谢酶和NO有关。
