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Influence of maternal protein malnutrition on oxidative stress and regulators of mitochondrial biogenesis in female rat hearts over succeeding generations

Silva, Severina Cássia Andrade, Braz, Glauber Rudá Feitoza, do Nascimento, Luciana Caroline Paulino, Santana, David Filipe, da Siva Pedroza, Anderson Apolonio, Silva, Tercya Lucidi Araujo, Fernandes, Mariana Pinheiro, Selliti, Donald F., Lagranha, Claudia Jacques
Life sciences 2019 v.232 pp. 116579
antioxidant activity, biogenesis, biomarkers, catalase, females, gene expression, heart, kwashiorkor, lipid peroxidation, mitochondria, moieties, nutrition, oxidation, oxidative stress, rats, sulfhydryl groups, superoxide dismutase, transcription (genetics), transcription factors
We sought to evaluate the effects of maternal protein restriction (LP) on oxidative balance and transcription factors for mitochondrial biogenesis in the hearts of young female rats of both the first (F1) and second (F2) generation.We evaluated oxidative stress biomarkers (lipid peroxidation and protein oxidation), enzymatic antioxidant defense (activity of superoxide dismutase-SOD, catalase, and glutathione-S-transferase-GST), nonenzymatic antioxidant defense (reduced glutathione-GSH and sulfhydryl groups) and gene expression of AMPK, PGC-1α and TFAM.Interestingly, lipid peroxidation was decreased (49%, p < 0.001) in the LP-F1 group and 59% (p < 0.001) in LP-F2. In enzymatic defense, we observed increases in SOD activity in the LP-F1 group (79%, p = 0.036) and in CAT activity (approximately 40%, p = 0.041). GSH was increased in F2 in both groups (LP 546%, p < 0.0001 and in NP 491.7%, p < 0.0001). With respect to mitochondrial biogenesis gene transcription, we observed a decrease in AMPK (60%, p < 0. 0001) and an increase in PGC-1α (340%, p < 0.001) in LP compared to NP in the F1 generation. TFAM was decreased in LP-F2L compared to NP-F2L (42%, p = 0.0069) and increased in LP-F2 compared to LP-F1 (160%, p = 0.0037).Our study contributes to knowledge of inheritance, showing that despite the potential mitochondrial ‘inheritance’ of cardiovascular damage caused by maternal malnutrition, that damage is not cross-generational and can be eliminated with proper nutrition in the F1 generation.