This study was undertaken to elucidate the role of anti- the specificity of this phenomenon is restricted to HPR.
Altogether, we provide the first direct evidence that HPR oxidants and oxidative stress in cell death induced by HPR.
We show that pharmacological doses of HPR, but not of other stimulates the generation of intracellular free radicals,
which appear to have a causative role in the induction of retinoids tested, rapidly elicit the formation of intracellular
free radicals, whose detoxification by antioxidants blocks the apoptosis in vitro. Our findings raise the possibility that apoptotic activity of the retinoid. These data raise the possibility the therapeutic efficacy of HPR may, at least in part, that the therapeutic effectiveness of HPR may, at least in part, depend on these apoptosis-inducing oxidative phenomena. depend on its pro-oxidative activity
This study was undertaken to elucidate the role of anti- the specificity of this phenomenon is restricted to HPR.Altogether, we provide the first direct evidence that HPR oxidants and oxidative stress in cell death induced by HPR.We show that pharmacological doses of HPR, but not of other stimulates the generation of intracellular free radicals,which appear to have a causative role in the induction of retinoids tested, rapidly elicit the formation of intracellularfree radicals, whose detoxification by antioxidants blocks the apoptosis in vitro. Our findings raise the possibility that apoptotic activity of the retinoid. These data raise the possibility the therapeutic efficacy of HPR may, at least in part, that the therapeutic effectiveness of HPR may, at least in part, depend on these apoptosis-inducing oxidative phenomena. depend on its pro-oxidative activity
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