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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 ...
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]
Crosslinking describes the process through which carbon-centered radicals on different chains combine to form a network of crosslinks. In contrast, chain scission occurs when a carbon-centered radical on the polymer backbone reacts with another free radical, typically from oxygen in the atmosphere, causing a break in the main chain. Free ...
He published his observations concerning the burns that developed that eventually healed, and misattributed them to ozone. Röntgen believed the free radical produced in air by X-rays from the ozone was the cause, but other free radicals produced within the body are now understood to be more important. David Walsh first established the symptoms ...
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 hydroxyl radical has a very short in vivo half-life of approximately 10 −9 seconds and a high reactivity. [5] This makes it a very dangerous compound to the organism. [6] [7] Unlike superoxide, which can be detoxified by superoxide dismutase, the hydroxyl radical cannot be eliminated by an enzymatic reaction.
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 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.