Kamsani, Y.S., Rajikin, M.H., Chatterjee, A., Nor-Ashikin, M.N.K. and Nuraliza, A.S
Present study investigated estrogen (E2), progester one (P4), malondialdehyde (MDA), glutathione peroxidase (GPx), catalase (CAT) and superoxide dis mutase (SOD) profiles in pregnant mice treated with nicotine concurrently with γ -tocotrienol ( γ -TCT), a non-enzymatic antioxidant. Ninety-six (6 - 8 weeks old) day 1 pc mice (Mus musculus) were inject ed(sc) with either 0.9% saline or nicotine of 3.0 mg/kg/day; or gavaged with γ -TCT alone of 60 mg/kg/day or treated with nicotine concurrently with γ - TCT from day 1 through day 7 pc. Nicotine did not a ffect implantation but reduced the count of intrauterine embryo and fetal survival rate. Concom itant treatment of nicotine concurrently with γ -TCT reversed the altered fetal parameters back to norma l. High levels of MDA with corresponding low levels of GPx, CAT and SOD in nicotine-induced plasma were also reversed. Nicotine-induced elevated levels of E2 with a corresponding decrease in P4 were also reverted. Gamma-TCT supplementation concurrently with nicotine seems to overcome the ef fects of nicotine on fetal development, fetal outcome as well as the survival rate of the newborn . The results of the present study show that foetal development and foetal outcome, also survival rate of the newborn in nicotine-treated mice are maintained by γ -TCT, a protective antioxidant, through combating f ree radicals generation in nicotine- induced oxidative stress.
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