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Abstract
In this paper we show the protective effect of folic acid on oxidative stress in offspring caused by chronic maternal ethanol consumption during pregnancy and the lactation period. Glutathione reductase (GR) specific activity was assayed in liver and pancreas of offspring and mothers. In the offspring, these tissues were also assayed for markers of oxidative damage to lipids and proteins. The results show that ethanol exposure during pregnancy and lactation increased the specific activity of GR in tissues of the mothers (32–34% increase) as well as in the liver of their progeny (24%). Thiobarbituric acid reactive substances (TBARS) were also increased in the liver and pancreas of 21-day-old rats (37- and 54%, respectively). Alcohol also increased the amount of carbonyl groups in proteins in both tissues. These measures of ethanol-mediated oxidative stress were mitigated when pregnant rats were treated with folic acid concomitantly to ethanol administration. The antioxidant capacity of folic acid seems to be involved in its protective effect. The results obtained in the present work suggest that folic acid may be useful in the prevention of damage and promotion of health of the progeny of ethanol-treated rats.