Ciftci Osman, Disli Olcay Murat, Timurkaan Necati
1Department of Pharmaceutical Toxicology, University of Inonu, Malatya, Turkey.
Toxicol Ind Health. 2013 Oct;29(9):806-11. doi: 10.1177/0748233712442735. Epub 2012 Apr 10.
2,3,7,8-Tetracholorodibenzo-p-dioxin (TCDD) is a highly toxic environmental contaminant that causes severe toxic effects in animal and human. In this study, we investigated the toxic effects of TCDD and the preventive effects of protocatechuic acid (PCA), a widespread phenolic compound, in the heart tissue of rats. For this purpose, 3-4 months old 28 rats with 280-310 g body weights were equally divided into 4 groups (control, TCDD, PCA, TCDD + PCA group). A 2 μg/kg dose of 2,3,7,8-TCDD and 100 mg/kg dose of PCA were dissolved in corn oil and given orally to the rats for 45 days. The results indicated that TCDD induced oxidative stress by increasing the level of thiobarbituric acid reactive substance and by decreasing the levels of glutathione, catalase, glutathione peroxidase and superoxide dismutase in the heart tissue of rats. In contrast, PCA treatment prevents the toxic effects of TCDD on oxidative stress. In addition, histopathological alterations such as necrosis and hemorrhage occurred in TCDD group, and PCA treatment partially prevents these alterations in heart tissue. In this study, it was concluded that TCDD exposure led to toxic effects in heart tissue and PCA treatment could prevent the toxicity of TCDD.
2,3,7,8-四氯二苯并对二恶英（TCDD）是一种剧毒的环境污染物，可对动物和人类造成严重的毒性影响。在本研究中，我们调查了TCDD的毒性作用以及原儿茶酸（PCA，一种广泛存在的酚类化合物）对大鼠心脏组织的预防作用。为此，将28只体重在280 - 310克、3 - 4月龄的大鼠平均分为4组（对照组、TCDD组、PCA组、TCDD + PCA组）。将2微克/千克剂量的2,3,7,8-TCDD和100毫克/千克剂量的PCA溶解于玉米油中，经口给予大鼠，持续45天。结果表明，TCDD通过增加大鼠心脏组织中硫代巴比妥酸反应性物质的水平以及降低谷胱甘肽、过氧化氢酶、谷胱甘肽过氧化物酶和超氧化物歧化酶的水平来诱导氧化应激。相比之下，PCA处理可预防TCDD对氧化应激的毒性作用。此外，TCDD组出现了坏死和出血等组织病理学改变，而PCA处理可部分预防心脏组织中的这些改变。在本研究中，得出的结论是，暴露于TCDD会导致心脏组织产生毒性作用，而PCA处理可预防TCDD的毒性。
