The Impact of a High Folic Acid and Low Vitamin B12 Diet on Oxidative Stress in Dams at Delivery and Young Offspring: Sex Matters.
Source: PubMed, NCBI / U.S. National Library of Medicine
Maternal micronutrient imbalances during pregnancy can interfere with fetal development by affecting oxidative stress pathways. Folic acid (FA) and vitamin B12, essential components of one-carbon metabolism, are especially crucial. This study examined the effects of a high-folic-acid and low-vitamin-B12 (HFALB12) diet on oxidative stress markers in pregnant mice and their offspring, with a focus on sex-specific responses. Female C57BL/6 mice were fed either a HFALB12 or a control (normal FA and B12) diet before and during pregnancy until weaning. Offspring were exposed to the same maternal diet post-weaning until 60-65 days of age. Total homocysteine (tHcy) was measured in plasma, while markers of oxidative stress-thiobarbituric acid reactive substances (TBARS), protein carbonyls, and glutathione (tGSH, rGSH, GSSG)-were assessed in placental and liver tissues of dams and in livers of adult offspring. Dams of the HFALB12 diet had significantly elevated tHcy, and their livers and placentas showed higher TBARS (p < 0.05). Offspring from the HFALB12 group were heavier at weaning than those from the control group. In adult offspring, HFALB12 exposure increased hepatic tGSH and GSSG; notably, only females showed elevated rGSH and reduced carbonyl content, indicating a sex-specific redox response. Results demonstrated that a maternal HFALB12 diet alters oxidative stress profiles in maternal livers and placentas, and in offspring tissues, as a consequence of a combined maternal and p
Abstract
Maternal micronutrient imbalances during pregnancy can interfere with fetal development by affecting oxidative stress pathways. Folic acid (FA) and vitamin B12, essential components of one-carbon metabolism, are especially crucial. This study examined the effects of a high-folic-acid and low-vitamin-B12 (HFALB12) diet on oxidative stress markers in pregnant mice and their offspring, with a focus on sex-specific responses. Female C57BL/6 mice were fed either a HFALB12 or a control (normal FA and B12) diet before and during pregnancy until weaning. Offspring were exposed to the same maternal diet post-weaning until 60-65 days of age. Total homocysteine (tHcy) was measured in plasma, while markers of oxidative stress-thiobarbituric acid reactive substances (TBARS), protein carbonyls, and glutathione (tGSH, rGSH, GSSG)-were assessed in placental and liver tissues of dams and in livers of adult offspring. Dams of the HFALB12 diet had significantly elevated tHcy, and their livers and placentas showed higher TBARS (p < 0.05). Offspring from the HFALB12 group were heavier at weaning than those from the control group. In adult offspring, HFALB12 exposure increased hepatic tGSH and GSSG; notably, only females showed elevated rGSH and reduced carbonyl content, indicating a sex-specific redox response. Results demonstrated that a maternal HFALB12 diet alters oxidative stress profiles in maternal livers and placentas, and in offspring tissues, as a consequence of a combined maternal and post-weaning diet, with enhanced redox adaptation in females. These findings support the concept of early sex-specific developmental programming in response to micronutrient imbalance before and after weaning.