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Cys could act as a defense mechanism not only for participating in PC biosynthesis but also directly as metal-chelator

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boulardii (1 10 9 CFU/day) was fed to a chronic renal failure model (nephrectomized rats) for 16-weeks trial and reduced blood urea nitrogen (BUN) levels and extended life were observed (Ranganathan et al., 2005)

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tBid translocates to the mitochondria, triggering cytochrome c release and subsequent activation of caspase-9 and caspase-3