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酸性媒介黄和橙黄Ⅱ诱导大鼠肝脏超微结构成分的脂质过氧化:与混合物的比较。

Lipid peroxidation of ultrastructural components of rat liver induced by metanil yellow and orange II: comparison with blend.

作者信息

Ramachandani S, Das M, Khanna S K

机构信息

Dyes and Food Adulterant Toxicology Laboratory, Industrial Toxicology Research Centre, Lucknow, India.

出版信息

Toxicol Ind Health. 1992 Jan-Apr;8(1-2):63-75. doi: 10.1177/074823379200800106.

Abstract

Metanil yellow and Orange II are extensively used in various industries and have not been included in the list of permitted food colours because of inadequate safety evaluation data. In this investigation the effect of Metanil yellow and Orange II on the lipid peroxidation in different subcellular fractions of liver was studied in order to understand the site of hepato-toxic potential and whether its blend has an additive, synergistic or antagonistic effect. Parenteral administration of Metanil yellow (80 mg/kg body weight) to rats for 3 days produced a highly significant (p less than 0.001) increase in NADPH-dependent enzymatic lipid peroxidation in nuclear (62%), mitochondrial (104%) and microsomal (54%) fractions. The same dose of Orange II to rats showed a relatively less but significant effect in nuclear (62%), mitochondrial (59%) and microsomal (38%) membranes. The blend of Metanil yellow and Orange II (40 mg + 40 mg/kg body weight) given intraperitoneally for 3 days resulted in either synergistic or additive effect in nuclear (122%), mitochondrial (130%), and microsomal (62%) membranes. The pro-oxidant free or FeSO4/ADP (1 mM/5 mM) or ascorbate (1 mM) dependent non-enzymatic lipid peroxidation in nuclear, mitochondrial and microsomal fractions was found to be enhanced by Metanil yellow to a greater extent as compared to Orange II, while the blend showed a synergistic or additive response. These results suggest that Metanil yellow and Orange II causes hepatic nuclear, mitochondrial and microsomal membrane damage and that the effect may be more severe with the use of blend.

摘要

金莲橙黄和橙黄II被广泛应用于各种行业,由于安全性评估数据不足,未被列入允许使用的食用色素清单。在本研究中,研究了金莲橙黄和橙黄II对肝脏不同亚细胞组分脂质过氧化的影响,以了解其肝毒性潜在作用部位以及它们的混合物是否具有相加、协同或拮抗作用。给大鼠腹腔注射金莲橙黄(80毫克/千克体重),连续3天,导致细胞核(62%)、线粒体(104%)和微粒体(54%)组分中依赖NADPH的酶促脂质过氧化显著增加(p小于0.001)。给大鼠注射相同剂量的橙黄II,在细胞核(62%)、线粒体(59%)和微粒体(38%)膜中显示出相对较小但显著的影响。腹腔注射金莲橙黄和橙黄II的混合物(40毫克 + 40毫克/千克体重),连续3天,在细胞核(122%)、线粒体(130%)和微粒体(62%)膜中产生协同或相加作用。与橙黄II相比,金莲橙黄在更大程度上增强了细胞核、线粒体和微粒体组分中游离或FeSO4/ADP(1毫摩尔/5毫摩尔)或抗坏血酸(1毫摩尔)依赖性非酶促脂质过氧化,而混合物显示出协同或相加反应。这些结果表明,金莲橙黄和橙黄II会导致肝细胞核、线粒体和微粒体膜损伤,并且混合物的影响可能更严重。

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