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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 mitochondrial theory of ageing has two varieties: free radical and non-free radical. The first is one of the variants of the free radical theory of ageing. It was formulated by J. Miquel and colleagues in 1980 [1] and was developed in the works of Linnane and coworkers (1989). [2] The second was proposed by A. N. Lobachev in 1978. [3]
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. [ 20 ] These include not only roles in apoptosis (programmed cell death) but also positive effects such as the induction of host defence [ 37 ] [ 38 ...
As part of their adaptation from marine life, terrestrial plants began producing non-marine antioxidants such as ascorbic acid (), polyphenols, and tocopherols.The evolution of angiosperm plants between 50 and 200 million years ago resulted in the development of many antioxidant pigments – particularly during the Jurassic period – as chemical defences against reactive oxygen species that ...
In pharmacology, the hormetic zone is similar to the therapeutic window. In the context of toxicology, the hormesis model of dose response is vigorously debated. [8] The biochemical mechanisms by which hormesis works (particularly in applied cases pertaining to behavior and toxins) remain under early laboratory research and are not well ...
It is also an important concept in both industrial chemistry and biology. [4] Autoxidation is therefore a fairly broad term and can encompass examples of photooxygenation and catalytic oxidation . The common mechanism is a free radical chain reaction , where the addition of oxygen gives rise to hydroperoxides and their associated peroxy ...
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.
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]