Fundamentally, when the production of ROS , hydroxyl radicals, singlet oxygen and RNS
and nitrogen dioxide radical NO2 does not exceed the capacity of endogenous antioxidant barriers in the body,
it performs beneficial functions which include: the control of gene expression,
regulation of cell signalling pathways, modulation of skeletal muscle
and defence against invading pathogens. In contrast,
when in excess and the activity of antioxidant defence is low, it potentially causes damage to cellular components,
induces harmful autoimmune responses and causes oxidative and/or nitrosative stress
In general, oxidative stress which is caused by an imbalance between the production of ROS
and antioxidant defence mechanisms in multicellular organism often leads to the modification of redox cell signalling and activation of pathways, and mechanisms involved in cardiovascular or chronic health problems
Fundamentally, when the production of ROS , hydroxyl radicals, singlet oxygen and RNSand nitrogen dioxide radical NO2 does not exceed the capacity of endogenous antioxidant barriers in the body, it performs beneficial functions which include: the control of gene expression, regulation of cell signalling pathways, modulation of skeletal muscle and defence against invading pathogens. In contrast, when in excess and the activity of antioxidant defence is low, it potentially causes damage to cellular components, induces harmful autoimmune responses and causes oxidative and/or nitrosative stress In general, oxidative stress which is caused by an imbalance between the production of ROS and antioxidant defence mechanisms in multicellular organism often leads to the modification of redox cell signalling and activation of pathways, and mechanisms involved in cardiovascular or chronic health problems
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