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For full versions of posted research articles readers are encouraged to email requests for "electronic reprints" (text file, PDF files, FAX copies) to the corresponding or lead author, who is highlighted in the posting.
___________________________________________
Wednesday, April 24, 2013
Ethanol- and/or Taurine-Induced Oxidative Stress in Chick Embryos
Because taurine alleviates ethanol- (EtOH-) induced lipid peroxidation and liver damage in rats, we asked whether exogenous taurine could alleviate EtOH-induced oxidative stress in chick embryos.
Exogenous EtOH (1.5 mmol/Kg egg or 3 mmol/Kg egg), taurine (4 mol/Kg egg), or EtOH and taurine (1.5 mmol EtOH and 4 mol taurine/Kg egg or 3 mmol EtOH and 4 mol taurine/Kg egg) were injected into fertile chicken eggs during the first three days of embryonic development (E0–2). At 11 days of development (midembryogenesis), serum taurine levels and brain caspase-3 activities, homocysteine (HoCys) levels, reduced glutathione (GSH) levels, membrane fatty acid composition, and lipid hydroperoxide (LPO) levels were measured.
Early embryonic EtOH exposure caused increased brain apoptosis rates (caspase-3 activities); increased brain HoCys levels; increased oxidative-stress, as measured by decreased brain GSH levels; decreased brain long-chain polyunsaturated levels; and increased brain LPO levels.
Although taurine is reported to be an antioxidant, exogenous taurine was embryopathic and caused increased apoptosis rates (caspase-3 activities); increased brain HoCys levels; increased oxidative-stress (decreased brain GSH levels); decreased brain long-chain polyunsaturated levels; and increased brain LPO levels.
Combined EtOH and taurine treatments also caused increased apoptosis rates and oxidative stress.
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