Abnormal Increase in the Expression Level of Proliferating Cell Nuclear Antigen (PCNA) in the Liver and Hepatic Injury in Rats with Dietary Cobalamin Deficiency

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  • NAKAO Motoyuki
    Department of Applied Biological Chemistry, Graduate School of Life and Environmental Sciences, Osaka Prefecture University
  • KONO Nozomi
    Department of Applied Biological Chemistry, Graduate School of Life and Environmental Sciences, Osaka Prefecture University
  • ADACHI Satoko
    Department of Applied Biological Chemistry, Graduate School of Life and Environmental Sciences, Osaka Prefecture University
  • EBARA Shuhei
    Department of Applied Biological Chemistry, Graduate School of Life and Environmental Sciences, Osaka Prefecture University
  • ADACHI Tetsuya
    Center for Research and Development of Bioresources, Osaka Prefecture University
  • MIURA Takumi
    Department of Applied Biological Chemistry, Graduate School of Life and Environmental Sciences, Osaka Prefecture University
  • YAMAJI Ryoichi
    Department of Applied Biological Chemistry, Graduate School of Life and Environmental Sciences, Osaka Prefecture University
  • INUI Hiroshi
    Department of Applied Biological Chemistry, Graduate School of Life and Environmental Sciences, Osaka Prefecture University Center for Research and Development of Bioresources, Osaka Prefecture University
  • NAKANO Yoshihisa
    Department of Applied Biological Chemistry, Graduate School of Life and Environmental Sciences, Osaka Prefecture University Center for Research and Development of Bioresources, Osaka Prefecture University

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  • Abnormal Increase in the Expression Level of Proliferation Cell Nuclear Antigen (PCNA) in the Liver and Hepatic Injury in Rats with Dietary Cobalamin Deficiency

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Abstract

Dietary cobalamin (Cbl; vitamin B12) deficiency resulted in severe growth retardation in rats, and body weight in the Cbl-deficient rats at 20 wk of age was significantly lower compared with the age-matched Cbl-sufficient control rats. In contrast, liver weight, when normalized to body weight, was greater in the Cbl-deficient rats than in the controls (p<0.05). The expression level of proliferating cell nuclear antigen (PCNA), a marker for cell proliferation, in the liver was significantly enhanced in the deficient rats, suggesting that cell proliferation is abnormally activated in the liver under Cbl-deficient conditions. In addition, plasma alanine aminotransferase (ALT) activity, a marker for hepatic injury, was also significantly elevated in the deficient rats. When L-carnitine, which is used clinically for the treatment of Cbl-deficient patients with methylmalonic aciduria, was administered to the Cbl-deficient rats by intraperitoneal injection twice per day for 2 wk (each 0.5 mmol), the amount of methylmalonic acid excreted into the urine was significantly reduced, and the plasma ALT activity was lowered to a normal level. However, the PCNA expression in the liver was barely influenced by the treatment with carnitine. In contrast, when the deficient rats were fed an L-methionine-supplemented diet (4 g of L-methionine per kg of the diet) for 2 wk, the increased expression of PCNA was normalized.

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