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Prenatal iron overload induces hepatic oxidative stress and ferroptosis in offspring mice
Yi Yan1, Qing Yang1, Yanqiu Zhu1,2
1College of Veterinary Medicine, Sichuan Agricultural University, Chengdu, 611130, Sichuan, PR China.
Insights
Excessive iron during pregnancy harms offspring, causing liver damage and ferroptosis. This study reveals how high iron levels impact infant development and organ health.
Area of Science:
- Biochemistry
- Developmental Biology
- Toxicology
Background:
- Iron is vital for development but toxic in excess, especially during pregnancy.
- Maternal nutrition significantly impacts offspring health and development.
Purpose of the Study:
- To investigate the effects of excessive maternal iron supplementation on offspring's hepatic health and ferroptosis.
- To assess changes in body weight, liver index, iron levels, antioxidant capacity, and ferroptosis markers in offspring.
Main Methods:
- Pregnant mice received varying iron doses.
- Offspring were analyzed for body weight, liver index, hepatic iron, antioxidant enzyme activity, and ferroptosis-related protein expression.
Main Results:
- Excess iron reduced offspring body and liver weights, causing liver abnormalities.
- Hepatic iron accumulation and oxidative stress were observed, with decreased antioxidant enzyme activity.
- Iron overload altered ferroptosis pathway proteins, increasing some and decreasing others like GPX4 and SLC7A11.
Conclusions:
- Excessive maternal iron leads to hepatic iron overload, oxidative stress, and ferroptosis in offspring.
- These changes highlight potential risks of high iron intake during pregnancy for infant liver health.
Abstract:
Iron is an essential micronutrient required for normal growth and development. However, excessive iron intake can exert toxic effects, particularly during sensitive developmental windows such as pregnancy. In this study, pregnant female mice were supplemented with varying concentrations of iron until day 21 post-delivery. On postnatal days 0 and 21, we assessed the body weight, liver index, hepatic iron content, antioxidant capacity, and expression of ferroptosis-related proteins in the offspring. Excessive maternal iron supplementation significantly decreased both body and liver weights of offspring and induced histopathological abnormalities in hepatic tissue. Liver iron levels were markedly elevated, accompanied by significant reductions in the activities of antioxidant enzymes including T-AOC, CAT, GSH-Px, and SOD, as well as decreased hepatic GSH content. Moreover, iron overload increased the protein expression levels of p-AMPKα/AMPKα, p-ULK1/ULK1, Beclin1, FTH1, and COX2, while decreasing the levels of SLC7A11, GPX4, and NCOA4. Collectively, these findings suggest that excessive iron supplementation during pregnancy leads to hepatic iron accumulation, oxidative stress, and ferroptosis in offspring mice.
