Search results
Results From The WOW.Com Content Network
Oxidative stress mechanisms in tissue injury. Free radical toxicity induced by xenobiotics and the subsequent detoxification by cellular enzymes (termination).. Oxidative stress reflects an imbalance between the systemic manifestation of reactive oxygen species and a biological system's ability to readily detoxify the reactive intermediates or to repair the resulting damage. [1]
Hydroxyl radicals can attack the deoxyribose DNA backbone and bases, potentially causing a plethora of lesions that can be cytotoxic or mutagenic. Cells have developed complex and efficient repair mechanisms to fix the lesions. In the case of free radical attack on DNA, base-excision repair is the repair mechanism used. Hydroxyl radical ...
Antioxidative stress is an overabundance of bioavailable antioxidant compounds that interfere with the immune system's ability to neutralize pathogenic threats. The fundamental opposite is oxidative stress, which can lead to such disease states as coronary heart disease or cancer.
Free radical toxicity induced by xenobiotics and the subsequent detoxification by cellular enzymes (termination). Effects of ROS on cell metabolism are well documented in a variety of species. [ 19 ] These include not only roles in apoptosis (programmed cell death) but also positive effects such as the induction of host defence [ 36 ] [ 37 ...
The free radical theory of aging states that organisms age because cells accumulate free radical damage over time. [1] A free radical is any atom or molecule that has a single unpaired electron in an outer shell. [2] While a few free radicals such as melanin are not chemically reactive, most biologically relevant free radicals are highly ...
The third substrate is Q, which accepts the second electron from the QH 2 and is reduced to Q.−, which is the ubisemiquinone free radical. The first two substrates are released, but this ubisemiquinone intermediate remains bound. In the second step, a second molecule of QH 2 is bound and again passes its first electron to a cytochrome c acceptor.
The hydroxyl radical can damage virtually all types of macromolecules: carbohydrates, nucleic acids , lipids (lipid peroxidation) and amino acids (e.g. conversion of Phe to m-Tyrosine and o-Tyrosine). The hydroxyl radical has a very short in vivo half-life of approximately 10 −9 seconds and a high reactivity. [5]
The relative importance of the antioxidant and pro-oxidant activities of antioxidant vitamins is an area of current research, but vitamin C, for example, appears to have a mostly antioxidant action in the body. [7] [9] However, less data is available for other dietary antioxidants, such as polyphenol antioxidants, [10] zinc, [11] and vitamin E ...