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  • Title: Antioxidant role of endogenous coenzyme Q against the ischemia and reperfusion-induced lipid peroxidation in fetal rat brain.
    Author: Tsukahara Y, Wakatsuki A, Okatani Y.
    Journal: Acta Obstet Gynecol Scand; 1999 Sep; 78(8):669-74. PubMed ID: 10468057.
    Abstract:
    BACKGROUND: Ischemia and subsequent reperfusion induce lipid peroxidation in the cerebrum of the fetal rat. The present study evaluated the antioxidant activity of endogenous coenzyme Q in protecting against the lipid peroxidation induced in the fetal rat brain by ischemia/reperfusion. METHODS: We used wistar rats at day 19 of pregnancy. Fetal ischemia was induced by bilateral occlusion of the utero-ovarian artery for 20 minutes. For reperfusion, the occlusion was released and the circulation was restored for 30 minutes. Control rats underwent sham operation. We determined the levels of thiobarbituric acid-reactive substances, the concentrations of coenzyme Q9, coenzyme Q10, and the mitochondrial respiratory control index in fetal brains. RESULTS: Occlusion for 20 minutes significantly reduced the respiratory control index (p < 0.01), but did not alter the levels of thiobarbituric acid-reactive substances, coenzyme Q9 or coenzyme Q10. Subsequent reperfusion, however, significantly increased the level of thiobarbituric acid-reactive substances (from 6.53+/-1.54 to 11.46+/-3.31 nM/mg of protein, p < 0.01) and significantly decreased the level of coenzyme Q9 (from 291.73+/-108.94 to 162.44+/-56.83 pM/mg of protein, p < 0.05) and that of coenzyme Q10 (from 153.10+/-75.24 to 79.84+/-30.40 pM/mg of protein, p < 0.05). The respiratory control index was still significantly lower following reperfusion than in controls (p < 0.01). Significant negative correlations were observed between the level of thiobarbituric acid-reactive substances and the concentrations of either coenzyme Q9 (r = -0.68, p < 0.001) or coenzyme Q10 (r = -0.70, p < 0.001). CONCLUSION: Endogenous coenzyme Q may protect the fetal rat brain against the lipid peroxidation induced by ischemia/reperfusion.
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