Traumatic brain injury and trichloroethylene exposure interact and produce functional, histological, and mitochondrial deficits
| Autor: | Andrew Sauerbeck, Randy L. Hunter, Patrick G. Sullivan, Guoying Bing |
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| Rok vydání: | 2012 |
| Předmět: |
Male
medicine.medical_specialty Mitochondrial Diseases Parkinson's disease Tyrosine 3-Monooxygenase Traumatic brain injury Substantia nigra Striatum Motor Activity Article Rotarod performance test Oxygen Consumption Developmental Neuroscience Internal medicine medicine Animals Dopamine transporter Dopamine Plasma Membrane Transport Proteins Movement Disorders biology Tyrosine hydroxylase Receptors Dopamine D2 business.industry medicine.disease Corpus Striatum Rats Inbred F344 Rats Trichloroethylene Disease Models Animal Endocrinology Gene Expression Regulation nervous system Neurology Dopamine receptor Brain Injuries Rotarod Performance Test Anesthesia Solvents biology.protein business |
| Zdroj: | Experimental Neurology. 234:85-94 |
| ISSN: | 0014-4886 |
| DOI: | 10.1016/j.expneurol.2011.12.012 |
| Popis: | Mitochondria play a pivotal role in the development of pathology associated with Parkinson's disease (PD), traumatic brain injury (TBI), and following exposure to the environmental toxin trichloroethylene (TCE). Evidence from humans indicates that both TBI and TCE can play a role in the development of PD and that each of these insults result in significant mitochondrial dysfunction. In the current studies we hypothesized that exposure to both TCE and TBI would result in increased pathology associated with PD. To test this hypothesis, 16 week old male Fischer 344 rats were administered TCE for either one or two weeks by oral gavage. Following exposure to TCE, rats were subjected to either a sham, mild (1.0mm), or moderate (2.0mm) controlled cortical impact TBI. Given the strong connection between mitochondrial function and PD, TBI, and TCE, tissue from the striatum and substantia nigra were analyzed 6h after the TBI. Neither TCE exposure, TBI, nor the combination of the two insults resulted in mitochondrial deficits at 6h post-TBI in the substantia nigra. Unlike the substantia nigra, the striatum exhibited significant mitochondrial dysfunction. Exposure to TCE alone for two weeks resulted in approximately a 75% reduction in mitochondrial function (p |
| Databáze: | OpenAIRE |
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