Antagonism by Taurine on the Ruthenium Red-Induced and 6-Hydroxydopamine Plus 1-Methyl-4-Phenylpyridinium-Induced Ca2+ Release from Rat Liver Mitochondria
Mitochondria have been implicated in the maintenance of the Ca2+ “set-point” in cells2,13,15, where control of Ca2+ levels plays a significant role in enzymatic regulation and energy production14,9,12,16,10. Pathological conditions that result in increased tissue Ca2+ concentration, e.g., ischemia, oxidative stress, excito- and neuro-toxicity, involve alterations in the continued ability of Ca2+-regulating organelles such as sarcolemma, mitochondria and sarcoplasmic reticulum, to provide long-term control of cellular Ca2+ levels (for review see 19, 20). The disruption of Ca2+ homeostasis with loss of accumulated Ca2+ possibly by opening a specific mitochondrial pore may account to some extent for the toxicity of 1-methyl-4-phenylpyridinium (MPP) and 6-hydroxydopamine (6-HD) that cause lesions similar to idiopathic Parkinson’s disease in primates6.
KeywordsMitochondrial Protein Liver Mitochondrion Taurine Concentration Membrane Permeability Transition Differential Absorbance
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