Dietary selenium protects against selected signs of aging and methylmercury exposure.
Dietary selenium protects against selected signs of aging and methylmercury exposure.
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DOI:
10.1016/j.neuro.2010.01.003
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发表时间:
2010-03
期刊:
影响因子:
3.4
通讯作者:
Newland MC
中科院分区:
文献类型:
--
作者:
Heath JC;Banna KM;Reed MN;Pesek EF;Cole N;Li J;Newland MC
Acute or short-term exposure to high doses of methylmercury (MeHg) causes a well-characterized syndrome that includes sensory and motor deficits. The environmental threat from MeHg, however, comes from chronic, low-level exposure, the consequences of which are poorly understood. Selenium (Se), an essential nutrient, both increases deposition of mercury (Hg) in neurons and mitigates some of MeHg's neurotoxicity in the short term, but it is unclear whether this deposition produces long-term adverse consequences. To investigate these issues, adult Long Evans rats were fed a diet containing 0.06 or 0.6 ppm of Se as sodium selenite. After 100 days on these diets, the subjects began consuming 0.0, 0.5, 5.0, or 15 ppm of Hg as methylmercuric chloride in their drinking water for 16 months. Somatosensory sensitivity, grip strength, hind-limb cross (clasping reflex), flexion, and voluntary wheel-running in overnight sessions were among the measures examined. MeHg caused a dose- and time-dependent impairment in all measures, No effects appeared in rats consuming 0 or 0.5 ppm of Hg. Somatosensory function, grip strength, and flexion were among the earliest signs of exposure. Selenium significantly delayed or blunted MeHgs effects. Selenium also increased running in unexposed animals as they aged, a novel finding that may have important clinical implications. Nerve pathology studies revealed axonal atrophy or mild degeneration in peripheral nerve fibers, which is consistent with abnormal sensorimotor function in chronic MeHg neurotoxicity. Lidocaine challenge reproduced the somatosensory deficits but not hind-limb cross or flexion. Together, these results quantify the neurotoxicity of long-term MeHg exposure, support the safety and efficacy of Se in ameliorating MeHg's neurotoxicity, and demonstrate the potential benefits of Se during aging.
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影响因子:
5.3
作者:
Lin, YW;Tseng, TJ;Hsieh, ST
通讯作者:
Hsieh, ST
影响因子:
8.8
作者:
Nakamura, T;Popitz-Bergez, F;Strichartz, GR
通讯作者:
Strichartz, GR
影响因子:
5.1
作者:
BAKIR, F;TIKRITI, S;SHIHRISTANI, H
通讯作者:
SHIHRISTANI, H
影响因子:
3.4
作者:
Newland, M. Christopher;Paletz, Elliott M.;Reed, Miranda N.
通讯作者:
Reed, Miranda N.
DOI:
10.1152/ajpregu.00396.2005
发表时间:
2005-12-01
影响因子:
2.8
作者:
Judge, S;Jang, YM;Leeuwenburgh, C
通讯作者:
Leeuwenburgh, C