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MitoQ supplementation prevent long-term impact of maternal smoking on renal development, oxidative stress and mitochondrial density in male mice offspring.

ABSTRACT: To investigate the effect of maternal MitoQ treatment on renal disorders caused by maternal cigarette smoke exposure (SE). We have demonstrated that maternal SE during pregnancy increases the risk of developing chronic kidney disease (CKD) in adult offspring. Mitochondrial oxidative damage contributes to the adverse effects of maternal smoking on renal disorders. MitoQ is a mitochondria-targeted antioxidant that has been shown to protect against oxidative damage-related pathologies in many diseases. Female Balb/c mice (8 weeks) were divided into Sham (exposed to air), SE (exposed to cigarette smoke) and SEMQ (exposed to cigarette smoke with MitoQ supplemented from mating) groups. Kidneys from the mothers were collected when the pups weaned and those from the offspring were collected at 13 weeks. Maternal MitoQ supplementation during gestation and lactation significantly reversed the adverse impact of maternal SE on offspring's body weight, kidney mass and renal pathology. MitoQ administration also significantly reversed the impact of SE on the renal cellular mitochondrial density and renal total reactive oxygen species in both the mothers and their offspring in adulthood. Our results suggested that MitoQ supplementation can mitigate the adverse impact of maternal SE on offspring's renal pathology, renal oxidative stress and mitochondrial density in mice offspring.

SUBMITTER: Sukjamnong S

PROVIDER: S-EPMC5919980 | biostudies-literature | 2018 Apr

REPOSITORIES: biostudies-literature

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MitoQ supplementation prevent long-term impact of maternal smoking on renal development, oxidative stress and mitochondrial density in male mice offspring.

Sukjamnong Suporn S Chan Yik Lung YL Zakarya Razia R Nguyen Long The LT Anwer Ayad G AG Zaky Amgad A AA Santiyanont Rachana R Oliver Brian G BG Goldys Ewa E Pollock Carol A CA Chen Hui H Saad Sonia S

Scientific reports 20180426 1

To investigate the effect of maternal MitoQ treatment on renal disorders caused by maternal cigarette smoke exposure (SE). We have demonstrated that maternal SE during pregnancy increases the risk of developing chronic kidney disease (CKD) in adult offspring. Mitochondrial oxidative damage contributes to the adverse effects of maternal smoking on renal disorders. MitoQ is a mitochondria-targeted antioxidant that has been shown to protect against oxidative damage-related pathologies in many disea ...[more]

PMID: 29700332

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Project description:BackgroundGenistein is a dietary supplement with phyto-estrogenic properties. Therefore, high intake of genistein during pregnancy may have adverse effects on the genetic integrity of testes and germ cells of male offspring. In this study, we examined whether maternal exposure to genistein during pregnancy induced oxidative DNA damage in the male germline at adolescence.MethodsAtm-ΔSRI mice have lower glucose-6-phosphate dehydrogenase (G6PDH) activity, which is important for maintaining levels of reduced glutathione and therefore these mice have an increased susceptibility to oxidative stress. Parental heterozygous Atm-ΔSRI mice received a genistein-rich or control diet, after which they were mated to obtain offspring. During pregnancy, mothers remained on the respective diets and after delivery all animals received control diets. Redox status and oxidative DNA damage were assessed in testes and sperm of 12 weeks old male offspring. Gene expression of Cyp1b1, Comt, and Nqo1 was assessed in testes, and DNA methylation as possible mechanism for transmission of effects to later life.ResultsIntake of genistein during pregnancy increased oxidative DNA damage in testes of offspring, especially in heterozygous Atm-ΔSRI mice. These increased DNA damage levels coincided with decreased expression of Comt and Nqo1. Heterozygous Atm-ΔSRI mice had higher levels of DNA strand breaks in sperm compared to wild type littermates, and DNA damage was further enhanced by a genistein-rich maternal diet. G6PDH activity was higher in mice with high maternal intake of genistein compared to control diets, suggesting compensation against oxidative stress. A positive correlation was observed between the levels of DNA methylation and oxidative DNA damage in testes.ConclusionThese data indicate that prenatal exposure to genistein altered gene expression and increased DNA damage in testes and sperm of adolescent male offspring. These effects of genistein on DNA damage in later life coincided with alterations in DNA methylation.

Project description:BackgroundContracting skeletal muscle produces reactive oxygen species (ROS) originating from both mitochondrial and cytosolic sources. The use of non-specific antioxidants, such as vitamins C and E, during exercise has produced inconsistent results in terms of exercise performance. Consequently, the effects of the mitochondrial-targeted coenzyme Q10, named Mitoquinone (MitoQ) on exercise responses are currently under investigation.MethodsIn this study, we conducted a meta-analysis to quantitatively synthesize research assessing the impact of MitoQ on aerobic endurance performance and exercise-induced oxidative damage. PubMed, Web of Science, and SCOPUS databases were used to select articles from inception to January 16th of 2024. Inclusion criteria were MitoQ supplementation must be compared with a placebo group, showing acute exercise responses in both; for crossover designs, at least 14 d of washout was needed, and exercise training can be concomitant to MitoQ or placebo supplementation if the study meets the other inclusion criteria points. The risk of bias was evaluated through the Critical Appraisal Checklist (JBI).ResultsWe identified eight studies encompassing a total sample size of 188 subjects. Our findings indicate that MitoQ supplementation effectively reduces exercise-induced oxidative damage (SMD: -1.33; 95% CI: -2.24 to -0.43). Furthermore, our findings indicate that acute and/or chronic MitoQ supplementation does not improve endurance exercise performance (SMD: -0.50; 95% CI: -1.39 to 0.40) despite reducing exercise-induced oxidative stress. Notably, our sensitivity analysis reveals that MitoQ may benefit subjects with peripheral artery disease (PAD) in improving exercise tolerance.ConclusionWhile MitoQ effectively reduces exercise-induced oxidative damage, no evidence suggests that aerobic exercise performance is enhanced by either acute or chronic MitoQ supplementation. However, acute MitoQ supplementation may improve exercise tolerance in subjects with PAD. Future research should investigate whether MitoQ supplementation concurrent with exercise training (e.g., 4-16 weeks) alters adaptations induced by exercise alone and using different doses.

Dataset Information

MitoQ supplementation prevent long-term impact of maternal smoking on renal development, oxidative stress and mitochondrial density in male mice offspring.

Publications

MitoQ supplementation prevent long-term impact of maternal smoking on renal development, oxidative stress and mitochondrial density in male mice offspring.

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