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硫代乙酰胺肝毒性中组织修复反应与剂量的关系。

Tissue repair response as a function of dose in thioacetamide hepatotoxicity.

作者信息

Mangipudy R S, Chanda S, Mehendale H M

机构信息

Division of Pharmacology and Toxicology, College of Pharmacy and Health Sciences, Northeast Louisiana University, Monroe 71209-0470, USA.

出版信息

Environ Health Perspect. 1995 Mar;103(3):260-7. doi: 10.1289/ehp.95103260.

DOI:10.1289/ehp.95103260
PMID:7768227
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1519068/
Abstract

The purpose of the present study was to establish a dose-response relationship for thioacetamide (TA), where tissue regeneration as well as liver injury were two simultaneous but opposing responses. Male Sprague-Dawley rats were injected intraperitioneally with a 12-fold dose range of TA, and both liver injury and tissue repair were measured. Liver injury was assessed by serum enzyme elevations. Serum alanine aminotransferase (ALT) elevation did not show any dose response over a 12-fold dose range up to 24 hr. A dramatic ALT elevation was evident after 24 hr and only for the highest dose (600 mg/kg). Tissue regeneration response was measured by 3H-thymidine (3H-T) incorporation into hepatocellular DNA and by proliferating cell nuclear antigen (PCNA) procedure during a time course (6, 12, 24, 36, 48, 72, and 96 hr). Tissue regeneration, as indicated by 3H-T incorporation, peaked at 36 hr after administration of a low dose of TA (50 mg/kg). With increasing doses, a greater but delayed stimulation of cell division was observed until a threshold was reached (300 mg/kg). Above the tissue repair threshold (600 mg/kg), because stimulated tissue repair as revealed by 3H-T incorporation in hepatonuclear DNA was significantly delayed and attenuated, injury assessed by serum enzyme elevations was remarkably accelerated, indicating unrestrained progression of injury leading to animal death. These findings suggest that, in addition to the magnitude of tissue repair response, the time at which this occurs is critical in restraining the progression of injury, thereby determining the ultimate outcome of toxicity.(ABSTRACT TRUNCATED AT 250 WORDS)

摘要

本研究的目的是建立硫代乙酰胺（TA）的剂量反应关系，其中组织再生和肝损伤是两个同时出现但相反的反应。将雄性Sprague-Dawley大鼠腹腔注射12倍剂量范围的TA，同时测量肝损伤和组织修复情况。通过血清酶升高评估肝损伤。在长达24小时的12倍剂量范围内，血清丙氨酸转氨酶（ALT）升高未显示任何剂量反应。24小时后，仅最高剂量（600mg/kg）出现明显的ALT升高。通过在肝细胞DNA中掺入3H-胸腺嘧啶核苷（3H-T）以及在时间进程（6、12、24、36、48、72和96小时）中采用增殖细胞核抗原（PCNA）程序来测量组织再生反应。以3H-T掺入表示的组织再生在给予低剂量TA（50mg/kg）后36小时达到峰值。随着剂量增加，观察到细胞分裂的刺激作用更大但延迟，直至达到阈值（300mg/kg）。高于组织修复阈值（600mg/kg）时，由于肝细胞核DNA中3H-T掺入所显示的受刺激组织修复明显延迟和减弱，血清酶升高评估的损伤显著加速，表明损伤不受控制地进展导致动物死亡。这些发现表明，除了组织修复反应的程度外，其发生的时间对于抑制损伤进展至关重要，从而决定毒性的最终结果。（摘要截断于250字）

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[THE EFFECT OF THIOACETYL COMPOUNDS ON THE LIVER PARENCHYMA IN THE ANIMAL EXPERIMENT].[硫代乙酰化合物在动物实验中对肝实质的影响]
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Isolation of pure and unaltered liver nuclei morphology and biochemical composition.分离出形态和生化组成纯净且未改变的肝细胞核。
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A Set of Six Gene Expression Biomarkers Identify Rat Liver Tumorigens in Short-term Assays.一组六个基因表达生物标志物可在短期检测中识别大鼠肝脏肿瘤发生源。
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