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质子诱导X射线发射(PIXE)分析及大鼠肝癌发生过程中的DNA链断裂研究:钒与β-胡萝卜素联合补充可能的化学预防作用

Proton-Induced X-ray Emission (PIXE) Analysis and DNA-chain Break study in rat hepatocarcinogenesis: A possible chemopreventive role by combined supplementation of vanadium and beta-carotene.

作者信息

Chattopadhyay Mitali Basu, Mukherjee Sutapa, Kulkarni Indira, Vijayan V, Doloi Manika, Kanjilal Nb, Chatterjee Malay

机构信息

Division of Biochemistry, Department of Pharmaceutical Technology Jadavpur University, Kolkata 700 032, India.

出版信息

Cancer Cell Int. 2005 May 26;5(1):16. doi: 10.1186/1475-2867-5-16.

DOI:10.1186/1475-2867-5-16
PMID:15918908
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1156919/
Abstract

Combined effect of vanadium and beta-carotene on rat liver DNA-chain break and Proton induced X-ray emission (PIXE) analysis was studied during a necrogenic dose (200 mg/kg of body weight) of Diethyl Nitrosamine (DENA) induced rat liver carcinogenesis. Morphological and histopathological changes were observed as an end point biomarker. Supplementation of vanadium (0.5 ppm ad libitum) in drinking water and beta-carotene in the basal diet (120 mg/Kg of body weight) were performed four weeks before DENA treatment and continued till the end of the experiment (16 weeks). PIXE analysis revealed the restoration of near normal value of zinc, copper, and iron, which were substantially altered when compared to carcinogen treated groups. Supplementation of both vanadium and beta-carotene four weeks before DENA injection was found to offer significant (64.73%, P < 0.001) protection against generation of single-strand breaks when compared with the carcinogen control counter parts. A significant stabilization of hepatic architecture of the cells was observed as compared to carcinogen control in vanadium plus beta-carotene treated group. This study thus suggests that vanadium, a prooxidant but potential therapeutic agent yield safe and effective pharmacological formulation with beta-carotene, an antioxidant, in the inhibition of experimental rat hepatocarcinogenesis.

摘要

在亚硝基二乙胺(DENA)诱导大鼠肝癌发生的致死剂量(200mg/kg体重)下,研究了钒和β-胡萝卜素对大鼠肝脏DNA链断裂及质子诱导X射线发射(PIXE)分析的联合作用。观察形态学和组织病理学变化作为终点生物标志物。在DENA处理前四周,在饮用水中补充钒(0.5ppm随意摄取),在基础饮食中补充β-胡萝卜素(120mg/kg体重),并持续至实验结束(16周)。PIXE分析显示,锌、铜和铁的含量恢复到接近正常水平,与致癌物处理组相比,这些元素的含量发生了显著变化。与致癌物对照组相比,在DENA注射前四周补充钒和β-胡萝卜素可显著(64.73%,P<0.001)保护细胞免受单链断裂的产生。与致癌物对照组相比,钒加β-胡萝卜素处理组的肝细胞结构显著稳定。因此,本研究表明,钒作为一种促氧化剂但潜在的治疗剂,与抗氧化剂β-胡萝卜素联合使用,可产生安全有效的药理学配方,用于抑制实验性大鼠肝癌发生。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/14ad/1156919/93ed8bcba5eb/1475-2867-5-16-6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/14ad/1156919/89321ba0c78e/1475-2867-5-16-1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/14ad/1156919/246644842e52/1475-2867-5-16-2.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/14ad/1156919/35eb77e84cce/1475-2867-5-16-4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/14ad/1156919/ce8d672fd085/1475-2867-5-16-5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/14ad/1156919/93ed8bcba5eb/1475-2867-5-16-6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/14ad/1156919/89321ba0c78e/1475-2867-5-16-1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/14ad/1156919/246644842e52/1475-2867-5-16-2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/14ad/1156919/c25cfa7ff98c/1475-2867-5-16-3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/14ad/1156919/35eb77e84cce/1475-2867-5-16-4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/14ad/1156919/ce8d672fd085/1475-2867-5-16-5.jpg
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