Melatonin prevents the formation of pyrrolized proteins in human plasma induced by hydrogen peroxide

Martinez-Cruz, Francisco; Guerrero, Juan M.; Osuna, Carmen

doi:10.1016/s0304-3940(02)00020-4

Cited by 15 publications

(12 citation statements)

References 19 publications

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“…An essential component of the apoptotic transduction pathway triggered by I/R is the intracellular generation of ROS. Melatonin has been found to protect cells from oxidative stress induced by a variety of free radical-generating agents and processes (43)(44)(45). In fact, melatonin displays the antioxidant properties and plays a critical role in preserving the functional integrity of membrane lipids (46).…”

Section: Discussionmentioning

confidence: 99%

Prevention of apoptotic and necrotic cell death, caspase‐3 activation, and renal dysfunction by melatonin after ischemia/reperfusion

et al. 2003

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The pineal hormone melatonin has been reported to protect tissue from oxidative damage. This study was designed to determine whether melatonin could prevent cell events leading to tissue injury and renal dysfunction after ischemia/reperfusion (I/R). Using an in vivo rat model of I/R, we show a significant increase in kidney malondialdehyde concentrations, reflecting lipid peroxidation, and cell apoptosis measured by TUNEL staining. This apoptotic cell death was associated with an increase in the activity of the proapoptotic factor caspase-3, determined by fluorometric protease activity assay. Histomorphological analysis of ischemic kidneys revealed that the most extensive tubular necrosis occurred at 24 and 48 h after reperfusion, which correlated with peak elevations in blood urea nitrogen and creatinine. Rat pretreatment with melatonin prevented lipid peroxidation, cell apoptosis, and necrosis and blocked caspase-3 activity. The prevention of tissue injury was associated with the improvement of renal function as shown by the decrease in blood urea nitrogen and creatinine concentrations. The demonstration that melatonin prevents postreperfusion apoptotic and necrotic cell death and improves renal function suggests that melatonin may represent a novel therapeutic approach for prevention of I/R injury.

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Section: Discussionmentioning

confidence: 99%

Prevention of apoptotic and necrotic cell death, caspase‐3 activation, and renal dysfunction by melatonin after ischemia/reperfusion

et al. 2003

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“…OLAARP formation is accepted as an ultimate step in the lipid peroxidation process, in the presence of proteins. Therefore, the detection of PP has been suggested to be used as a marker of OS [4,5] .…”

Section: Discussionmentioning

confidence: 99%

“…Serum PP levels were determined using Ehrlich's reagent [p-(dimethylamino) benzaldehyde; DMAB] by the method of Hidalgo et al [4] , modified by Martinez-Cruz et al [5] . The principle was based on the measurement of color intensity of Ehrlich adducts at 570 nm, resulted from the interaction of pyrroles on proteins and DMAB under high temperature and acidic conditions.…”

Section: Biochemical Analysismentioning

confidence: 99%

“…The principle was based on the measurement of color intensity of Ehrlich adducts at 570 nm, resulted from the interaction of pyrroles on proteins and DMAB under high temperature and acidic conditions. The evaluation was made by extinction coefficient of 35.000 M -1 cm -1 of ε-Npyrrolylnorleucine as standard, and PP values were expressed in nano moles per mg protein determined at 280 nm (n mol/mg protein) [5] .…”

Section: Biochemical Analysismentioning

confidence: 99%

“…For instance, pyrrolized protein (PP), formed widely in the reaction of protein amino groups with lipid peroxidation products such as MDA, lipid hydroperoxide (LHP), epoxyl-and hydroxyl-alkenals, has been proposed as can be used as a marker in demonstrating the exposure to OS [4,5] .…”

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confidence: 99%

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The Effect of N-acetylcysteine on Pyrrolized Protein, Lipid Hydroperoxide and Thiol Levels in the Carbon Tetrachloride Hepatotoxicity

Yazıcı¹,

Köse²

2016

ijps

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Yazici, et al.: N-acetylcysteine Effect on Oxidative Stress in RatsThis study was performed, on the rat model, to form oxidative stress by carbon tetrachloride and to reveal the relationship between toxicity and oxidative/thiol stresses through lipid/protein oxidation and to investigate the effects of N-acetylcysteine on the hepatotoxicity induced oxidative stress. Wistar albino male rats were divided into four groups as carbon tetrachloride, N-acetylcysteine, carbon tetrachloride-N-acetylcysteine and control, each of ten rats. Carbon tetrachloride (1.0 ml, 800 mg/kg; single dose) and N-acetylcysteine (200 mg; three doses) were intraperitoneally applied to corresponding groups as per kg of rat weight. Hepatotoxicity was identified with histopathological methods. Besides the thiol levels in plasma/tissue samples, pyrrolized protein and total lipid hydroperoxide levels in serum samples were measured. Carbon tetrachloride-induced hepatotoxic lesions remarkably improved in the presence of N-acetylcysteine. There was no significant difference between control and N-acetylcysteine groups, in terms of parameters measured in serum/plasma and tissue samples. When compared to these groups, pyrrolized protein and total lipid hydroperoxide levels were found to be higher; whereas plasma/tissue thiol levels lower in the carbon tetrachloride group. N-acetylcysteine in combination with carbon tetrachloride significantly lowered pyrrolized protein and total lipid hydroperoxide levels, and increased thiol levels, so that the values were reached to those of control and N-acetylcysteine groups. As reflected by higher pyrrolized protein and total lipid hydroperoxide, and lower thiol levels, enhanced free radical production in the carbon tetrachloride hepatotoxicity may lead to oxidative and thiol stresses mediated lipid/protein oxidation. In addition, N-acetylcysteine, a powerful antioxidant, may be added as a thiol source to the treatment protocols of several diseases whose pathogenesis is of oxidative and thiol stress.

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A novel approach in psoriasis: first usage of known protein oxidation markers to prove oxidative stress

et al. 2016

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Oxidative stress may play a pivotal role in the pathogenesis of psoriasis, an inflammatory/hyperproliferative skin disease characterized by the cutaneous accumulation of neutrophils releasing reactive oxygen species, as revealed in a number of studies. This study was performed to demonstrate the presence of oxidative stress in psoriasis, as measured by protein oxidation markers. Twenty-nine psoriasis patients were selected based on disease severity assessment using body surface area as well as the psoriasis area severity index (PASI), and were grouped as mild (PASI ≤ 10) and moderate-to-severe (PASI > 10). The measured parameters in psoriatic patients and fourteen healthy volunteers were as follows: erythrocyte sedimentation rate (ESR), high sensitive C-reactive protein (CRP), myeloperoxidase (MPO) activity, neopterin, total lipid hydroperoxides (LHP), pyrrolized protein (PP), protein carbonyl compounds (PCC), advanced oxidation protein products (AOPP), thiol levels, along with complete blood count. Except lower thiols, all parameters were found to be higher in total patients as well as in subgroups, compared to controls. There was no significant difference among the subgroups. In conclusion, protein oxidation in psoriatics, not only in moderate-to-severe, but also in mild patients, may be explained by the findings of inflammation, phagocytic cell oxidation, and MPO-hypochlorous acid-oxidation reactions; as reflected by increased total/differential leucocytes counts, CRP, ESR as well as MPO, neopterin, AOPP, PCC, PP, LHP, and decreased thiol levels. Demonstrating the AOPP and PP formation for the first time, oxidants from active neutrophils/monocytes may play an important role in the pathogenesis of psoriasis, leading to oxidative stress, especially by protein oxidation.

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Melatonin prevents the formation of pyrrolized proteins in human plasma induced by hydrogen peroxide

Cited by 15 publications

References 19 publications

Prevention of apoptotic and necrotic cell death, caspase‐3 activation, and renal dysfunction by melatonin after ischemia/reperfusion

Prevention of apoptotic and necrotic cell death, caspase‐3 activation, and renal dysfunction by melatonin after ischemia/reperfusion

The Effect of N-acetylcysteine on Pyrrolized Protein, Lipid Hydroperoxide and Thiol Levels in the Carbon Tetrachloride Hepatotoxicity

A novel approach in psoriasis: first usage of known protein oxidation markers to prove oxidative stress

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