Long-term exposure to bisphenol A or S promotes glucose intolerance and changes hepatic mitochondrial metabolism in male Wistar rats
| Autor: | Maria Fernanda Hornos Carneiro, Cecília Cristina de Souza Rocha, Carlos Roberto Porto Dechandt, Luciane C. Alberici, Fernando Barbosa, Lara Ferreira Azevedo |
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| Rok vydání: | 2019 |
| Předmět: |
Male
endocrine system medicine.medical_specialty Mitochondria Liver Oxidative phosphorylation Mitochondrion Toxicology Mitochondrial Dynamics Oxidative Phosphorylation Phenols Internal medicine medicine Animals Glucose homeostasis Sulfones Benzhydryl Compounds Beta oxidation urogenital system Chemistry Body Weight Organ Size General Medicine Metabolism Glucose Tolerance Test Lipids Rats ESPÉCIES REATIVAS DE OXIGÊNIO Mitochondrial respiratory chain Endocrinology Mitochondrial biogenesis Mitochondrial fission Energy Metabolism Reactive Oxygen Species Oxidation-Reduction hormones hormone substitutes and hormone antagonists Food Science |
| Zdroj: | Repositório Institucional da USP (Biblioteca Digital da Produção Intelectual) Universidade de São Paulo (USP) instacron:USP |
| ISSN: | 0278-6915 |
| Popis: | The present study evaluates the effects of low-level long-term exposure to bisphenol A (BPA) and bisphenol S (BPS) on serum biochemical markers, glucose homeostasis, mitochondrial energy metabolism, biogenesis and dynamics, and redox status in livers of Wistar rats. While only the exposure to BPS induces a significant body mass gain after 21 weeks, both compounds alter serum lipid levels and lead to the development of glucose intolerance. Regarding mitochondrial metabolism, both bisphenols augment the electron entry by complex II relative to complex I in the mitochondrial respiratory chain (MRC), and reduce mitochondrial content; BPA reduces OXPHOS capacity and uncouples respiration (relative to maximal capacity of MRC) but promotes a significant increase in fatty acid oxidation. Either exposure to BPA or BPS leads to an increase in mitochondrial-derived reactive oxygen species, mainly at complex I. Additionally, BPA and BPS significantly upregulate the expression levels of dynamin-related protein 1 related to mitochondrial fission, while BPA downregulates the expression of proliferator-activated receptor gamma coactivator 1 alpha, a master regulator of mitochondrial biogenesis. In summary, our data shows that exposure to both compounds alters metabolic homeostasis and mitochondrial energy metabolism, providing new mechanisms by which BPA and BPS impair the mitochondrial metabolism. |
| Databáze: | OpenAIRE |
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