TITLE

An Investigation on Protective Effects of Vitamin E Against Lipopolysaccharide-induced Fetal Injuries in Rat

AUTHOR(S)
Delashoub, Masoud; Khojasteh, Seyed Mahdi Banan
PUB. DATE
July 2012
SOURCE
Advances in Environmental Biology;Jul2012, Vol. 6 Issue 8, p2274
SOURCE TYPE
Academic Journal
DOC. TYPE
Article
ABSTRACT
Lipopolysaccharide (LPS) has been associated with adverse developmental outcome, including intra-uterine fetal death (IUFD), embryonic resorption, intra-uterine growth retardation (IUGR) and preterm delivery in rodents. Induced toxicity in these organs is related to production of reactive oxygen species (ROS). Vitamin E is a fat soluble vitamin that has antioxidant effects. In this study, we investigated the effect of vitamin E on LPS-induced IUFD and IUGR in rat. First pregnant rats were selected and were divided to 4 groups. All pregnant rats except controls received an intraperitoneal (75 µg/kg) injection of LPS daily on gestation day (gd) 15-17. The second and third groups received 20 mg/kg-1 of vitamin E (I.M) daily since 7 days before of first injection of LPS. On gd 18, the number of live fetuses, dead fetuses and resorption sites was counted. Live fetuses in each litter were weighted. Crown-rump and tail lengths were examined and skeletal development was evaluated. Also maternal liver, placenta and fetal liver samples were excised for measurement of TBARS and GSH contents. Results were agreed with other researches and showed that maternally administered LPS significantly increased fetal mortality, decreased fetal weight and crown-rump and tail lengths of live fetuses and retarded skeletal ossification in caudal vertebrae, anterior and posterior phalanges, and supraoccipital bone. Biochemical and anatomical results in co-treatment of vitamin E and LPS are close to control group that demonstrate pre-treatment of vitamin E decrease toxicity of LPS in rat fetuses. All of this suggests that vitamin E protects against LPS-induced fetal death and reversed LPS-induced growth and skeletal development retardation via counteracting LPS-induced oxidative stress.
ACCESSION #
90477967

 

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