Oxidative stress is recognized as a trigger of different metabolic events in all organisms. Various factors correlated with oxidation, such as the -oxidation of fatty acids and their enzymatic or nonenzymatic byproducts (e.g., precocious sexual inducer factors and lipoperoxides) have been shown to be involved in aflatoxin formation. In the present study, we found that increased levels of reactive oxygen species (ROS) were correlated with increased levels of aflatoxin biosynthesis in Aspergillus parasiticus. To better understand the role of ROS formation in toxin production, we generated a mutant (⌬ApyapA) having the ApyapA gene deleted, given that ApyapA orthologs have been shown to be part of the antioxidant response in other fungi. Compared to the wild type, the mutant showed an increased susceptibility to extracellular oxidants, as well as precocious ROS formation and aflatoxin biosynthesis. Genetic complementation of the ⌬ApyapA mutant restored the timing and quantity of toxin biosynthesis to the levels found in the wild type. The presence of putative AP1 (ApYapA orthologue) binding sites in the promoter region of the regulatory gene aflR further supports the finding that ApYapA plays a role in the regulation of aflatoxin biosynthesis. Overall, our results show that the lack of ApyapA leads to an increase in oxidative stress, premature conidiogenesis, and aflatoxin biosynthesis.Reactive oxygen species (ROS), such as superoxide anionand lipoperoxides (LOOH), which are formed from unsaturated fatty acids and can be produced in the cell during metabolic processes, can be overproduced following the action of oxidative stressors present in the environment (32,49,57). To counteract the potentially dangerous accumulation of ROS, cells have evolved strategies (49, 61) based on enzymatic or nonenzymatic systems (28,45). The main antioxidant enzymes in cells involved in ROS removal are superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPX). If H 2 O 2 exceeds the cell-scavenging capacity, it can generate highly reactive HO ⅐ through a Fenton reaction, which initiates the formation of LOOH in the membrane lipids (32). When ROS accumulation occurs, the oxidant/antioxidant balance is perturbed, which can damage the cell membrane and cell metabolism (free-radical theory of aging) (26). ROS produced at certain time points during the cell's life cycle and at low physiological concentrations play a crucial role in the organism's homeostasis and cell functions. As second messengers, ROS take part in the plant's developmental processes (18,24,31) and in the defense mechanisms against pathogens and abiotic stress (5, 24, 52, 62). Similar effects have been shown in mammals, where ROS at proper levels stimulate antioxidant reactions, immune system modulation, and regulation of cell proliferation (3,4,55,59,65). One of the major objectives of studying the biology of stress is to identify the key factors that control the switch from cytoprotective responses to cell dysfunction following oxidative insult (11)....
Carotenoids are used for systemic photoprotection in humans. Regarding mechanisms underlying photoprotective effects of carotenoids, here we compared the modulation of UVA-related injury by carotenoids. Human dermal fibroblasts (HDF) were exposed to moderate doses of UVA, which stimulated apoptosis, increased levels of reactive oxygen species and thiobarbituric acid reactive substances, decreased antioxidant enzymes activities, promoted membrane perturbation, and induced the expression of heme oxygenase-1 (HO-1). The carotenoids astaxanthin (AX), canthaxanthin (CX) and beta-carotene (betaC) were delivered to HDF 24 h before exposure to UVA. Astaxanthin exhibited a pronounced photoprotective effect and counteracted all of the above-mentioned UVA-induced alterations to a significant extent. beta-Carotene only partially prevented the UVA-induced decline of catalase and superoxide dismutase activities, but it increased membrane damage and stimulated HO-1 expression. Moreover, betaC dose-dependently induced caspase-3 activity following UVA exposure. In contrast, CX had no effect on oxidative damage, except for HO-1 expression, which was augmented. Uptake of AX by fibroblasts was higher than that of the other two carotenoids. The photostability of the three compounds in fibroblasts was AX > CX >> betaC. The data indicate that the oxo-carotenoid AX has a superior preventive effect towards photo-oxidative changes in cell culture.
UV-induced DNA damage can lead to melanoma, the most dangerous form of skin cancer. Understanding the mechanisms employed by melanocytes to protect against UV is therefore a key issue. In melanocytes, catalase is the main enzyme responsible for degrading hydrogen peroxide and we have previously shown that that low basal levels of catalase activity are associated with the light phototype in in vitro and ex vivo models. Here we investigate the possible correlation between its activity and melanogenesis in primary cultures of human melanocytes. We show that while the total melanin concentration is directly correlated to the level of pigmentation, the more the degree of pigmentation increased, the lower the proportion of pheomelanin present. Moreover, in human melanocytes in vitro, catalase-specific mRNA, protein and enzymatic activity were all directly correlated with total cellular melanin content. We also observed that immediately after a peroxidative treatment, the increase in reactive oxygen species was inversely associated with pigmentation level. Darkly pigmented melanocytes therefore possess two protective strategies represented by melanins and catalase activity that are likely to act synergistically to counteract the deleterious effects of UV radiation. By contrast, lightly pigmented melanocytes possess lower levels of melanogenic and catalase activity and are therefore more susceptible to accumulate damage after UV exposition.
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