Di(2-ethylhexyl)phthalate Alters the Synthesis and β-Oxidation of Fatty Acids and Hinders ATP Supply in Mouse Testes via UPLC-Q-Exactive Orbitrap MS-Based Metabonomics Study
| Autor: | Wenlian Yu, Wenping Xie, Wei Liu, Haishan Li, Yuan Cui, Huiming Chen, Lili Zhou, Guolin Shen, Wentao Li |
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| Rok vydání: | 2017 |
| Předmět: |
Male
endocrine system medicine.medical_specialty 010501 environmental sciences Endocrine Disruptors 01 natural sciences Mass Spectrometry 03 medical and health sciences chemistry.chemical_compound Mice 0302 clinical medicine Adenosine Triphosphate Internal medicine Diethylhexyl Phthalate Testis medicine Animals Metabolomics Receptor Chromatography High Pressure Liquid 0105 earth and related environmental sciences 030219 obstetrics & reproductive medicine Testicular atrophy Chemistry Fatty Acids Phthalate General Chemistry medicine.disease Citric acid cycle Mice Inbred C57BL Metabolic pathway Endocrinology Endocrine disruptor Biochemistry Gluconeogenesis General Agricultural and Biological Sciences Adenosine triphosphate Oxidation-Reduction |
| Zdroj: | Journal of agricultural and food chemistry. 65(24) |
| ISSN: | 1520-5118 |
| Popis: | Di(2-ethylhexyl) phthalate (DEHP) is considered to be an environmental endocrine disruptor at high levels of general exposure. Studies show that DEHP may cause testicular toxicity on human being. In this study, metabonomics techniques were used to identify differential endogenous metabolites, draw the network metabolic pathways, and conduct network analysis, to determine the underlying mechanisms of testicular toxicity induced by DEHP. The results showed that DEHP inhibited synthesis and accelerated β-oxidation of fatty acids and impaired the tricarboxylic acid cycle (TCA cycle) and gluconeogenesis, resulting in lactic acid accumulation and an insufficient ATP supply in the microenvironment of the testis. These alterations led to testicular atrophy and, thus, may be the underlying causes of testicular toxicity. DEHP also inhibited peroxisome proliferator activated receptors in the testis, which may be another potential reason for the testicular atrophy. These findings provided new insights to better understand the mechanisms of testicular toxicity induced by DEHP exposure. |
| Databáze: | OpenAIRE |
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