Adverse effect of oxidation

There are a variety of physiological, cellular and biochemical mechanisms that exist to ensure that the organism can generally effectively counter the adverse effects of oxidative insults. 

The adverse effects of oxidation, however, can be minimized by the use of oxidation inhibitors (referred to as antioxidants). Indeed, the commercialization of PP, and its use for outdoor applications, would... 

Carotenoid oxidation products are also supposed to have detrimental effects in vivo. As mentioned earlier, they are suspected to be involved in the adverse effects of high doses of 3-carotene supplementation in smokers and asbestos workers (CARET and ATBC studies) and in smoke-exposed ferrets. The mechanisms potentially involved have been investigated in vitro. P-Apo-8 -carotenal, an eccennic cleavage oxidation product of P-carotene, was shown to be a strong inducer of CYPlAl in rats, whereas P-carotene was not active. Cytochrome P450 (CYP 450) enzymes thus induced could enhance the activation of carcinogens and the destruction of retinoic acid. ... 

These results may be viewed in the wider context of interactions between potential ligands of multifunctional xenobiotics and metal cations in aquatic environments and the subtle effects of the oxidation level of cations such as Fe. The Fe status of a bacterial culture has an important influence on synthesis of the redox systems of the cell since many of the electron transport proteins contain Fe. This is not generally evaluated systematically, although the degradation of tetrachloromethane by a strain of Pseudomonas sp. under denitrifying conditions clearly illustrated the adverse effect of Fe on the biotransformation of the substrate (Lewis and Crawford 1993 Tatara et al. 1993). This possibility should therefore be taken into account in the application of such organisms to bioremediation programs. 

As organisms grew in size, the time for development and their lifetimes became much longer. This lifestyle, if it was to survive, demanded increased protection from the adverse effects of the environment and from other species and even from its own kind. Oxidation and the new catalysts for oxidising reactions were added to the... 

Nitrous oxide exerts a variety of its adverse effects by oxidizing vitamin Bn and rendering it inactive as a coenzyme in many essential metabolic processes. One vitamin dependent enzyme in particular, methionine synthetase, is involved in cell division and is necessary for DNA production. Adverse reproductive and hematologic effects caused by nitrous oxide are thought to be due to inactivation or dysfunction of methionine synthetase resulting in impairment of cell division. 

However, the adverse effects of APAP bioactivation are not observed until high doses are administered, where there is sufficient depletion of natural reserves of antioxidants, for example, reduced glutathione (GSH). Depletion of GSH exacerbates arylation of cellular proteins by NAPQI and amplifies oxidative stress from ROS, eventually leading to a drop in cellular ATP levels and cell death. Hence it is not the advent of covalent binding of reactive intermediates that is solely responsible for APAP toxicity, but rather a combination of events in which protein binding plays an important role. 

Taking into account the important role of balance in oxidant-antioxidant phenomena for human health and interrelation between internal and external factors, evaluation of oxidant-antioxidant state of human body fluids and natural resources of antioxidants is essential for therapy and prevention of diseases and adverse effects of environment. Thus, analysis of ready-made food and production processes monitoring are of great importance. 

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