{"title":"Differential behaviour of cell membranes towards iron-induced oxidative damage and the effects of melatonin.","authors":"P L Tang, M F Xu, Z M Qian","doi":"10.1159/000109140","DOIUrl":null,"url":null,"abstract":"<p><p>The ability of melatonin to protect iron-induced lipid peroxidation was studied in various rat cell membranes. The concentration of cellular membrane malondialdehyde (MDA) was used as an index of induced oxidative membrane damage. Cell membranes from the brain, heart, kidney and liver of the male Sprague-Dawley rat were incubated with ferric ammonium citrate (20 microg/ml iron) alone for 3 h and concomitant with varying concentrations of melatonin ranging from 125 to 2,000 microM. The basal MDA levels of all the cell membranes were 25.0+/-1.4 (brain), 21.2+/-0.2 (heart), 10.0+/-0.9 (kidney) and 20.7+/-0.4 (liver) microM/g membrane protein, and the highest lipid peroxidation after exposure to iron occurred in the kidney (314.4%), followed by the heart (151.3%), the liver (130.4%) and the brain (121.7%). This peroxidative effect was completely (ED50 846.7 microM for the heart) and partially suppressed by melatonin (ED50 462.1 microM for the brain, 178.3 microM for the kidney and 886.6 microM for the liver). This inhibition effect on MDA production by these cell membranes was also found - except for the liver - if melatonin was used alone. These results show that the direct effect of lipid peroxidation on cellular membrane following iron exposure is markedly reduced by melatonin.</p>","PeriodicalId":9265,"journal":{"name":"Biological signals","volume":"6 4-6","pages":"291-300"},"PeriodicalIF":0.0000,"publicationDate":"1997-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000109140","citationCount":"12","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Biological signals","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1159/000109140","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 12
Abstract
The ability of melatonin to protect iron-induced lipid peroxidation was studied in various rat cell membranes. The concentration of cellular membrane malondialdehyde (MDA) was used as an index of induced oxidative membrane damage. Cell membranes from the brain, heart, kidney and liver of the male Sprague-Dawley rat were incubated with ferric ammonium citrate (20 microg/ml iron) alone for 3 h and concomitant with varying concentrations of melatonin ranging from 125 to 2,000 microM. The basal MDA levels of all the cell membranes were 25.0+/-1.4 (brain), 21.2+/-0.2 (heart), 10.0+/-0.9 (kidney) and 20.7+/-0.4 (liver) microM/g membrane protein, and the highest lipid peroxidation after exposure to iron occurred in the kidney (314.4%), followed by the heart (151.3%), the liver (130.4%) and the brain (121.7%). This peroxidative effect was completely (ED50 846.7 microM for the heart) and partially suppressed by melatonin (ED50 462.1 microM for the brain, 178.3 microM for the kidney and 886.6 microM for the liver). This inhibition effect on MDA production by these cell membranes was also found - except for the liver - if melatonin was used alone. These results show that the direct effect of lipid peroxidation on cellular membrane following iron exposure is markedly reduced by melatonin.
研究了褪黑素在大鼠不同细胞膜中对铁诱导的脂质过氧化的保护作用。以细胞膜丙二醛(MDA)浓度作为诱导氧化膜损伤的指标。将雄性Sprague-Dawley大鼠的大脑、心脏、肾脏和肝脏细胞膜与柠檬酸铁铵(20微克/毫升铁)单独孵育3小时,并同时使用不同浓度的褪黑激素(125至2000微米)。各组细胞膜MDA基础水平分别为25.0+/-1.4(脑)、21.2+/-0.2(心)、10.0+/-0.9(肾)和20.7+/-0.4(肝)μ m /g膜蛋白,铁暴露后脂质过氧化率最高的部位为肾(314.4%),其次为心脏(151.3%)、肝脏(130.4%)和脑(121.7%)。这种过氧化作用完全被褪黑激素(心脏ED50为846.7微米)和部分被褪黑激素(大脑ED50为462.1微米,肾脏ED50为178.3微米,肝脏ED50为886.6微米)抑制。如果单独使用褪黑激素,还发现这些细胞膜对丙二醛产生的抑制作用(肝脏除外)。这些结果表明,褪黑激素显著降低了铁暴露后细胞膜脂质过氧化的直接作用。