mortality/aging
• in mice treated with D-galactosamine (GalN) and TNFalpha
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reproductive system
• in mice treated with D-galactosamine (GalN) and TNFalpha
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cellular
• in mouse embryonic fibroblasts treated with TNFalpha, cycloheximide (CHX), or CoCl2 (a chemical inducer of HIF-1)
• however, treatment with reactive oxygen species scavengers prevents induced cell death
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• in mouse embryonic fibroblasts
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• in mouse embryonic fibroblasts
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• in mice treated with D-galactosamine (GalN) and TNFalpha
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• mice treated with D-galactosamine (GalN) and TNFalpha exhibit increased apoptosis in the liver and testes compared with similarly treated wild-type mice
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• in mice treated with D-galactosamine (GalN) and TNFalpha
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• mouse embryonic fibroblasts treated with TNFalpha plus cycloheximide (CHX), and CoCl2 (a chemical inducer of HIF-1) exhibit increased reactive oxygen species compared with similarly treated wild-type cells
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liver/biliary system
• in mice treated with D-galactosamine (GalN) and TNFalpha
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homeostasis/metabolism
• in mice treated with D-galactosamine (GalN) and TNFalpha
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