Ferroptosis: a critical mechanism of N6-methyladenosine modification involved in carcinogenesis and tumor progression
Qingqing WeiChangning XueMengna LiJianxia WeiLemei ZhengShipeng ChenYumei DuanHongyu DengFaqing TangWei XiongMing Zhou
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Lipid peroxidation in microsomes prepared from liver of mice was initiated by NADPH, ascorbic acid and ferrous ions. The presence of Ca2+ modulated the lipid peroxidation in all these three systems. The mode and magnitude depend on the system and concentration of cofactors used for initiation of lipid peroxidation. In ascorbate system, Ca2+ enhanced the lipid peroxidation up to 30 microM concentration of ascorbic acid and beyond 30 microM concentration it inhibited. Ca2+ increased NADPH-dependent lipid peroxidation at all concentrations. Depending on concentration of Fe2+, lipid peroxidation was either decreased or increased in presence of Ca2+. It suggested that the in vitro findings may be cautiously extrapolated to the animal systems. In absence of cofactors, Ca2+ enhanced lipid peroxidation. EGTA inhibited Ca2+-enhanced lipid peroxidation. However in presence of ionophore A23187, Ca2+ potentiated lipid peroxidation. Since Ca2+ has a closed-shell electronic state and lacks electronic transitions, it may not participate directly in lipid peroxidation process. The effect of Ca2+ on lipid peroxidation may be through some biochemical processes or its interactions with membranes leading to various changes in their characteristics.
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Malondialdehyde
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Malondialdehyde
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Epigenetic alterations during aging are manifested with altered gene expression linking it to lifespan regulation, genetic instability, and diseases. Diet and epigenetic modifiers exert a profound effect on the lifespan of an organism by modulating the epigenetic marks. However, our understanding of the multifactorial nature of the epigenetic process during aging and the onset of disease conditions as well as its reversal by epidrugs, diet, or environmental factors is still mystifying. This review covers the key findings in epigenetics related to aging and age-related diseases. Furthermore, it holds a discussion about the epigenetic clocks and their implications in various age-related disease conditions, including cancer. Although, epigenetics is a reversible process, how fast the epigenetic alterations can revert to normal is an intriguing question. Therefore, this article touches on the possibility of utilizing nutrition and mesenchymal stem cell secretome to accelerate the epigenetic reversal and emphasizes the identification of new therapeutic epigenetic modifiers to counter epigenetic alteration during aging.
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Oxidative stress is associated with carcinogenesis. Reactive oxygen and nitrogen species contribute to the accumulation of mutations in the genome, presumably followed by selective processes. Recent data suggest that preferred signaling pathways exist for oxidative stress–associated carcinogenesis. Whether this completely depends on random mutations induced by reactive species or whether instead some fragile genomic loci are sensitive to oxidative damage in association with changes of transcriptional activity or other topologic or nontopologic effects remains to be explored. Reliable markers for oxidative stress as well as for oxidative stress–induced preneoplastic lesions must be established.
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Carcinogenesis is a stepwise process of accumulation of genetic and epigenetic abnormalities that can lead to cellular dysfunction. It has become clear that epigenetic changes are equally important for this multistep process to produce its results. This article describes the different roles that epigenetic modulation may play during carcinogenesis and how an early detection and chemopreventive intervention strategy that takes both sides of the equation into account would be advantageous.
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[The effect of nutritional factors on lipid peroxidation in the microsomes of rats of varying ages].
5-month- (mature) and 24-month-old (old) male Wag rats were examined for lipid peroxidation products and antioxidant enzymes activity in the liver cytosol. Imbalanced rations are shown to contribute to enhancement of lipid peroxidation entailing accumulation of lipid peroxidation products and inhibition of antioxidant enzymatic activity. Enrichment of food with antioxidant vitamins and fibers leads to lowering of age-related peroxidation.
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Objective To study the effect of high arsenic water on lipid peroxidation and anti-lipid peroxidation for clarifying the danger and the pathogenetic mechanism. Methods The SOD, GSH-Px, GSH and LPO of different age groups were measured and analysed. Results The higher the level of water arsenic, the higher the activity of SOD in serum was, especially in the 36 to 55 age groups, but the LPO level was significantly lower than the control group(P 0.05). The GSH level was higher than that in higher water arsenic area (P 0.05). The activity of GSH-Px 55 in age control group of 55 and above was higher than high water arsenic area. Conclusions Drinking high water arsenic could affect the system of lipid peroxidation and anti-lipid peroxidation, causing lipid peroxidation and damage to the body and compensative increase of anti-lipid peroxidation.
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When rat brain homogenate was incubated without adding iron, lipid peroxidation occurred temperature dependently between 27 degrees C and 42 degrees C. When homogenates of liver and heart were incubated under the same conditions, lipid peroxidation did not occur. The brain, compared with other organs, seems to be very vulnerable to oxidative damage with fever. Catalase promoted lipid peroxidation. The ability of dihydrolipoic acid and alpha-tocopherol to inhibit lipid peroxidation was very weak. In contrast, iron chelators, such as bathophenanthroline, desferrioxamine and EDTA, strongly inhibited lipid peroxidation, indicating that endogenous iron is involved in lipid peroxidation. Dialysis of brain homogenate depressed the temperature-dependent lipid peroxidation by about 30%. Then, the iron content of the homogenate decreased by about 35%. On the other hand, dialysis of EDTA-treated homogenate completely depressed the lipid peroxidation and the iron content of the homogenate decreased by about 87%. Adding iron to the homogenate dialyzed after EDTA treatment remarkably increased the lipid peroxidation, but the peroxidation reaction proceeded temperature independently. Our results suggest that endogenous iron, which may bind to cell components, causes temperature dependent lipid peroxidation by a site-specific mechanism.
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