Intraamniotic Ethyl Docosahexaenoate Administration Protects Fetal Rat Brain from Ischemic Stress

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Abstract
Studies were conducted on the prenatal rat given a single intraamniotic injection of ethyl docosahexaenoate (Et‐DHA; 9.6–12 mmol per fetus) or subjected to an n‐3 fatty acid‐deficient diet to assess the role of docosahexaenoate on oxidative stress during episodes of ischemia. A time‐dependent decrease in the ability of brain slices from animals treated with Et‐DHA to produce thiobarbituric acid‐reactive substance (TBARS), most pronounced after 1 day (from 58.1 ± 4.22 to 15.9 ± 1.6 nmol/mg of DNA), was noticed on stimulation with Fe2+. Brain slices from fetuses treated for 1 day with Et‐DHA and those from untreated fetuses produced TBARS levels of 46.7 ± 6.5 and 114.8 ± 10.8 nmol/mg of DNA, respectively, after a 20‐min occlusion of the fetal‐maternal circulation at embryonic day 20, suggesting a protective effect of Et‐DHA. The protective effect of a single dose of Et‐DHA in utero remained high up to 3 days after injection (p < 0.001) and was long‐lasting, yet not significant, up to 3 days following birth. In agreement with a reduction in TBARS production by slices, the endogenous levels of TBARS in brains of Et‐DHA‐treated animals were lower than in the controls. Et‐DHA‐injected fetuses exhibited significantly higher levels of esterified DHA than the non‐injected controls. n‐3‐deficient diet given to dams for 2 weeks before birth did not affect the levels of TBARS production in control fetal brain slices but abolished the increase caused by ischemia. Et‐DHA administration for 24 h to n‐3‐deficient fetuses reduced the amount of TBARS produced by the fetal brain slices from 49.1 ± 8.5 to 31.7 ± 4.1 nmol/mg of DNA. A protective effect from oxidative damage after postischemic oxidative stress in fetal brain following DHA supplements is suggested, whereas the effect of n‐3 fatty acid deficiency in this regard is more ambiguous.

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