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Department of Nutrition and Food Sciences, Fu-Jen University, Hsin-Chuang, Taiwan, Republic of China
2To whom correspondence should be addressed. E-mail: rweifen{at}mails.fju.edu.tw
This study was designed to determine whether nutritional folate
depletion exerts hepatic oxidative stress in relation to elevated
plasma homocysteine. To mimic various extents of folate depletion
status in vivo, male Wistar rats were fed an amino acid–defined diet
containing either 8 (control), 2, 0.5, or 0 mg folic acid/kg diet.
After a 4-wk feeding period, the plasma and hepatic folate
concentrations of the rats decreased significantly with each decrement
of dietary folate. Folate depletion did not significantly affect two
major liver antioxidants: reduced glutathione and 
-tocopherol.
Conversely, folate depletion decreased Cu-Zn superoxide dismutase
and glutathione peroxidase activities, but had no effect on catalase
activity in liver homogenates. Lipid peroxidation products, as measured
by thiobarbituric acid–reactive substances, were significantly higher
in livers of folate-depleted rats than in those of the controls.
This occurrence of hepatic oxidative stress in folate-depleted rats
was confirmed by demonstrating an increased susceptibility of livers of
folate-depleted rats to lipid peroxidation induced by additional
H2O2 or Fe2+ treatments compared
with the controls. Decreasing dietary folate intake resulted in graded
increases in plasma homocysteine concentrations of folate-depleted
rats. Elevated plasma homocysteine and decreased plasma and hepatic
folate concentrations in folate-depleted rats were all strongly and
significantly correlated with increased liver lipid peroxidation
(|r| 
0.58, P
< 0.0003). These data demonstrate that folate depletion and
elevated plasma homocysteine promote oxidative stress in rat livers.
KEY WORDS: • folate depletion • plasma homocysteine • oxidative stress • rats
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