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首页> 外文期刊>Life sciences >Dietary nucleotides have cytoprotective properties in rat liver damaged by thioacetamide.
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Dietary nucleotides have cytoprotective properties in rat liver damaged by thioacetamide.

机译：饮食核苷酸在大鼠肝脏中具有被硫代乙酰胺破坏的细胞保护特性。

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摘要

Liver cirrhosis has been induced with thioacetamide administered via different routes in rats and other species. The oral intake of thioacetamide causes nodular liver cirrhosis in rats characterized by extensive fibrosis occupying most of the hepatic parenchyma. To characterize the cytological features of cirrhosis induced by thioacetamide, and the degree of recovery obtained with dietary nucleotides, we made a morphometric study of the hepatocytes in rats administered 300 mg/l of thioacetamide for 4 months, and in rats receiving the same hepatotoxic treatment but allowed a 2-weeks recovery period on a nucleotide-free diet or a 250 mg/100 g nucleotide-supplemented diet. Thioacetamide caused to cell damage and affected the ultrastructure of hepatocytes leading to a decrease in cytoplasmic area together with increased nuclear and nucleolar size. Dietary supplementation with nucleotides favoured recovery, restoring the cytoplasmic (TN=491.7+/-9.6 vs TAA=305.1+/-3.7), nuclear (73.6+/-2.8 vs 97.4+/-2.9), and nucleolar area of damaged hepatocytes (5.6+/-0.3 vs 14.0+/-0.9). The injury from thioacetamide intake increased liver collagen, but dietary nucleotides prevented hepatic deposition of this protein. This study supports the hypothesis that dietary supplementation with nucleotides is decisive in ensuring hepatocyte recovery after thioacetamide-induced liver damage, and that dietary nucleotides have antifibrotic properties.
机译：在大鼠和其他物种中，硫代乙酰胺通过不同途径给予肝硬化。口服硫代乙酰胺会导致大鼠结节性肝硬化，其特征是广泛的纤维化占据了肝实质的大部分。为了表征由硫代乙酰胺诱发的肝硬化的细胞学特征以及饮食核苷酸获得的恢复程度，我们对给予300 mg / l硫代乙酰胺的大鼠和接受相同肝毒性治疗的大鼠的肝细胞进行了形态学研究但在无核苷酸饮食或补充250 mg / 100 g核苷酸的饮食中可以有2周的恢复期。硫代乙酰胺引起细胞损伤并影响肝细胞的超微结构，从而导致细胞质面积的减少以及核和核仁大小的增加。饮食中补充核苷酸有利于恢复，恢复受损的肝细胞的细胞质（TN = 491.7 +/- 9.6 vs TAA = 305.1 +/- 3.7），核（73.6 +/- 2.8 vs 97.4 +/- 2.9）和受损肝细胞的核仁面积（ 5.6 +/- 0.3与14.0 +/- 0.9）。硫代乙酰胺摄入引起的损伤增加了肝脏胶原蛋白，但饮食核苷酸阻止了该蛋白的肝沉积。这项研究支持以下假设：饮食中补充核苷酸对确保硫代乙酰胺诱导的肝损伤后肝细胞的恢复具有决定性作用，并且饮食中的核苷酸具有抗纤维化特性。

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