Effect of boric acid on oxidative stress in rats with fetal alcohol syndrome

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Sogut I., Oglakci A., Kartkaya K., Ol K., Sogut M. S., KANBAK G., ...More

EXPERIMENTAL AND THERAPEUTIC MEDICINE, vol.9, no.3, pp.1023-1027, 2015 (SCI-Expanded) identifier identifier

  • Publication Type: Article / Article
  • Volume: 9 Issue: 3
  • Publication Date: 2015
  • Doi Number: 10.3892/etm.2014.2164
  • Journal Indexes: Science Citation Index Expanded (SCI-EXPANDED)
  • Page Numbers: pp.1023-1027
  • Keywords: boric acid, catalase, fetal alcohol syndrome, glutathione peroxidase, malondialdehyde, superoxide dismutase, ETHANOL-METABOLISM, DIETARY BORON, CONSUMPTION, EXPOSURE, BRAIN
  • Dokuz Eylül University Affiliated: No


To the best of our knowledge, this is the first study concerning the effect of boric acid (BA) administration on fetal alcohol syndrome (FAS). In this study, the aim was to investigate prenatal alcohol-induced oxidative stress on the cerebral cortex of newborn rat pups and assess the protective and beneficial effects of BA supplementation on rats with FAS. Pregnant rats were divided into three groups, namely the control, alcohol and alcohol + boric acid groups. As markers of alcohol-induced oxidative stress in the cerebral cortex of the newborn pups, malondialdehyde (MDA), superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPx) levels were measured. Although the MDA levels in the alcohol group were significantly increased compared with those in the control group (P<0.05), the MDA level in the alcohol + boric acid group was shown to be significantly decreased compared with that in the alcohol group (P<0.01). The CAT activity of the alcohol + boric acid group was significantly higher than that in the alcohol group (P<0.05). The GPx activity in the alcohol group was decreased compared with that in the control group (P<0.05). These results demonstrate that alcohol is capable of triggering damage to membranes of the cerebral cortex of rat pups and BA could be influential in antioxidant mechanisms against oxidative stress resulting from prenatal alcohol exposure.