Organ Toxicity and Mechanisms

Archives of Toxicology

, Volume 81, Issue 7, pp 489-493

First online:

Activation of mitogen activated protein kinase (MAPK) during carbon tetrachloride intoxication in the rat liver

  • Chinatsu IidaAffiliated withDepartment of Food Science and Nutrition, Nara Women’s University
  • , Kozue FujiiAffiliated withDepartment of Food Science and Nutrition, Nara Women’s University
  • , Terumi KishiokaAffiliated withDepartment of Food Science and Nutrition, Nara Women’s University
  • , Ritsuko NagaeAffiliated withDepartment of Food Science and Nutrition, Nara Women’s University
  • , Yuki OnishiAffiliated withDepartment of Food Science and Nutrition, Nara Women’s University
  • , Ikuyo IchiAffiliated withDepartment of Food Science and Nutrition, Nara Women’s University
  • , Shosuke KojoAffiliated withDepartment of Food Science and Nutrition, Nara Women’s University Email author 

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Abstract

Carbon tetrachloride (CCl4: 4 ml/kg body weight as a 1:1 mixture of CCl4 and mineral oil) was orally administered to rats. After 12 h the activity of plasma AST (aspartate aminotransferase) and ALT (alanine aminotransferase) was significantly higher than that of the control group and plasma AST and ALT activities increased thereafter. These results indicated that the necrotic process was active at about 12 h and developed thereafter. After 2–24 h of CCl4 administration, the hepatic level of vitamin C, the most sensitive indicator of oxidative stress, decreased significantly, indicating that oxidative stress was significantly enhanced as early as 2 h after CCl4 intoxication and thereafter. Phosphorylated JNK (c-Jun NH2-terminal kinase) and phospho-ERK1/2 (extracellular signal-regulated kinase1/2) were significantly increased transiently 1–3 h after treatment with CCl4, while phosphorylated p38 decreased significantly 1–24 h after CCl4 treatment. These results indicated that the change in MAPKs (mitogen activated protein kinases) slightly preceded that in vitamin C, the most sensitive chemical indicator of oxidative stress.

Keywords

Carbon tetrachloride CCl4 ERK JNK MAPK Necrosis Oxidative stress P38 Vitamin C