Abstract
Mitochondria-targeted antioxidant 10-(6-plastoquinonyl)decyltriphenyl-phosphonium (SkQ1) as well as insulin and the inhibitor of glycogen-synthase kinase, Li(+) are shown to (i) protect renal tubular cells from an apoptotic death and (ii) diminish mitochondrial fission (the thread-grain transition) induced by ischemia/reoxygenation. However, SkQ1 and LiCl protected the mitochondrial reticulum of skin fibroblasts from ultraviolet-induced fission but were ineffective in preventing a further cell death. This means that mitochondrial fission is not essential for apoptotic cascade progression.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Animals
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Antioxidants / pharmacology*
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Apoptosis* / drug effects
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Cytoprotection*
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Enzyme Inhibitors / pharmacology
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Epithelium / drug effects
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Epithelium / radiation effects
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Epithelium / ultrastructure
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Fibroblasts / drug effects
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Fibroblasts / radiation effects
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Fibroblasts / ultrastructure
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Glycogen Synthase Kinases / antagonists & inhibitors
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Insulin / pharmacology*
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Kidney Tubules / drug effects
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Kidney Tubules / radiation effects
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Kidney Tubules / ultrastructure
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Lithium Chloride / pharmacology*
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Mitochondria / drug effects
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Mitochondria / radiation effects
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Mitochondria / ultrastructure*
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Oxygen / metabolism
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Plastoquinone / analogs & derivatives*
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Plastoquinone / pharmacology
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Rats
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Skin / drug effects
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Skin / radiation effects
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Skin / ultrastructure
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Ultraviolet Rays
Substances
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10-(6'-plastoquinonyl)decyltriphenylphosphonium
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Antioxidants
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Enzyme Inhibitors
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Insulin
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Glycogen Synthase Kinases
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Lithium Chloride
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Plastoquinone
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Oxygen