2011
DOI: 10.1016/j.ejphar.2010.09.033
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The cytotoxic mechanism of malondialdehyde and protective effect of carnosine via protein cross-linking/mitochondrial dysfunction/reactive oxygen species/MAPK pathway in neurons

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Cited by 94 publications
(76 citation statements)
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“…Resulting free radical chain reactions may cause membrane phospholipid disruption, in particular in cancer cells, where protecting mechanisms against intracellular oxidative stress have been reported to be altered [14]. In addition, endproducts of lipid peroxidation, such as malondialdehyde (MDA), may induce cell apoptosis by the formation of DNA adducts, such as pyrimido [1,2-a]purin-10(3H)-one, and subsequent DNA misrepair [15,16]. In clinical conditions, however, it is not certain that the administration of commercially available lipid emulsions can produce the same cytotoxic effect on cancer cells as free u-3 PUFAs.…”
Section: Introductionmentioning
confidence: 99%
“…Resulting free radical chain reactions may cause membrane phospholipid disruption, in particular in cancer cells, where protecting mechanisms against intracellular oxidative stress have been reported to be altered [14]. In addition, endproducts of lipid peroxidation, such as malondialdehyde (MDA), may induce cell apoptosis by the formation of DNA adducts, such as pyrimido [1,2-a]purin-10(3H)-one, and subsequent DNA misrepair [15,16]. In clinical conditions, however, it is not certain that the administration of commercially available lipid emulsions can produce the same cytotoxic effect on cancer cells as free u-3 PUFAs.…”
Section: Introductionmentioning
confidence: 99%
“…Administration of CARN lowered the level of secondary products of lipid peroxidation in plasma measured as TBARS. Cheng (Cheng et al, 2011) showed that CARN, but not other conventional antioxidants, could protect neurons against MDA-induced injury through decomposition of protein crosslinking and may serve as a novel agent in the treatment of neurodegenerative diseases. The "anti-carbonyl" effect of CARN administration was also evidenced by other authors (Aldini et al, 2010).…”
Section: Hpvmentioning
confidence: 99%
“…[105][106][107][108][109] Markers of cellular oxidative stress include malondialdehyde (a lipid peroxidation end product), F2-isoprostanes, and lipid hydroperoxide. 108 On the other hand, sleep related breathing disorders, especially OSA, disrupt the balance between ROS removal and formation to initiate oxidative stress, [110][111] and thus constitute another indirect pathogenesis of sleep apnea-associated CKD.…”
Section: Oxidative Stressmentioning
confidence: 99%