Acute effects of vanadate oligomers on heart, kidney, and liver histology in the Lusitanian toadfish (Halobatrachus didactylus)
Acute effects of vanadate oligomers on heart, kidney, and liver histology in the Lusitanian toadfish (Halobatrachus didactylus)
复制标题
DOI：
10.1007/s00244-003-2155-1
复制
发表时间：
2003-10-01
影响因子：
4
通讯作者：
Aureliano, M
中科院分区：
文献类型：
--
作者：
Borges, G;Mendonça, P;Aureliano, M
在Halobrachus didactylus的心脏、肾脏和肝脏中分析了钒酸盐低聚物对钒急性组织学效应的贡献（Schneider，1801）。以偏钒酸盐（含有邻位和位变异构体）或十钒酸盐（仅含有十异构体）的形式通过腹腔注射给予亚致死剂量的钒（5 mM，1 mL/kg），并将H.在注射后第1天和第7天处死双趾。用苏木精-伊红染色心室、肾脏和肝脏组织切片，并通过光学显微镜检查以确定钒诱导的组织损伤。另外。通过双偏振光显微镜分析苦皮酸染色的心室切片，以确定心室壁结构元件（胶原蛋白I、胶原蛋白III和心肌）占据的心肌部分。两种钒酸盐溶液在肾组织中产生类似的作用。形态学改变包括肾小管受损，表现为上皮细胞处于不同坏死状态。还观察到重吸收肾小管和深染间质组织。肝组织呈现深染和肥大的细胞核，沿着坏死和肥大的肝细胞，并且在暴露于十钒酸盐的肝脏中观察到更严重的变化。钒酸盐低聚物促进肾脏和肝脏中的明显组织病变，但不促进心脏组织中的明显组织病变。然而，心脏组织结构发生了变化。例如，十钒酸盐由于胶原纤维占据的心肌百分比降低而诱导心室肥大。一般来说，十钒酸盐比偏钒酸盐毒性更大。
The contribution of vanadate oligomers to the acute histological effects of vanadium was analyzed in the heart, kidney, and liver of Halobatrachus didactylus (Schneider, 1801). A sublethal vanadium dose (5 mM, 1 mL/kg) in the form of metavanadate (containing ortho and metameric species) or in the form of decavanadate (containing only decameric species) was intraperitoneally administered by injection, and specimens of H. didactylus were sacrificed at one and seven days postinjection. Sections of heart ventricle and renal and hepatic tissue were stained with hematoxylin-eosin and examined by light microscopy to identify vanadium-induced tissue injury. In addition. PicroSirius-stained ventricular sections were analyzed by bipolarized light microscopy to determine the fraction of myocardium occupied by the ventricular wall structural elements (collagen I, collagen III, and cardiac muscle). Both vanadate solutions produced similar effects in the renal tissue. Morphological alterations included damaged renal tubules showing disorganized epithelial cells in different states of necrosis. Reabsorbed renal tubules and hyperchromatic interstitial tissue were also observed. The hepatic tissue presented hyperchromatic and hypertrophied nuclei, along with necrotic and hypertrophied hepatocytes, and more severe changes were observed in the liver with exposure to decavanadate. Vanadate oligomers promoted evident tissue lesions in the kidney and liver, but not in the cardiac tissue. However, cardiac tissue structural changes were produced. For example, decavanadate induced a hypertrophy of the ventricle due to a decrease in the percentage of myocardium occupied by collagen fibers. In general, decavanadate was shown to be more toxic than metavanadate.