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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]
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 ...
According to the free radical theory of aging, oxidative damage initiated by reactive oxygen species is a major contributor to the functional decline that is characteristic of aging.
Senescence (/ s ɪ ˈ n ɛ s ə n s /) or biological aging is the gradual deterioration of functional characteristics in living organisms. Whole organism senescence involves an increase in death rates or a decrease in fecundity with increasing age, at least in the later part of an organism's life cycle.
Drug metabolism is the metabolic breakdown of drugs by living organisms, usually through specialized enzymatic systems. More generally, xenobiotic metabolism (from the Greek xenos "stranger" and biotic "related to living beings") is the set of metabolic pathways that modify the chemical structure of xenobiotics, which are compounds foreign to an organism's normal biochemistry, such as any drug ...
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 ...
After years of frustration over his inability to increase maximum lifespan with antioxidant supplements, Harman came to the conclusion that mitochondria were producing as well as being damaged by free radicals, but that exogenous antioxidants don't enter the mitochondria. And that it is mitochondria that determine lifespan.