Zinc and liver cirrhosis: Biochemical and histopathologic assessment

Dashti, H.; Mathew, T.C.; Jadaon, Mehrez M.; Ashkanani, Eman

doi:10.1016/s0899-9007(96)00403-0

Cited by 45 publications

(54 citation statements)

References 17 publications

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“…Histochemical survey of zinc/ethanol-treated liver sections by PAS reaction in the present study showed fair amount of glycogen content, while the histoenzymological survey of ATPase and SDH tests showed moderate to strong activity of these two enzymes which came in accordance with some previous studies [9,43,66]. This was explained by the guarding role of zinc against the ethanol-induced mechanisms discussed by some previous authors [28,37,44] who suggested an ethanol-mediated failure of metabolic pathways especially ATP production.…”

Section: Discussionsupporting

confidence: 92%

“…Also, this could be explained according to one previous report [67] who claimed that alcohol would induce the release of bacterial endototxin from gut which might cause inflammatory cells infiltration which would compress the sinusoids, while alcohol induced release of endothelins from sinusoidal endothelium would diminish sinusoidal lumen by the vasoconstrictive effect on perisinusoidal stellate cells. Additionally, the stroma was presumably injured as what had been inferred before by Dashti et al [66] that zinc supplementation to cirrhotic liver leads to decrease in fibrin, reticulin and collagen and concluded that zinc is needed not only to protect against acute ethanol injury but also to treat even late stages of alcoholic liver injury as fibrosis and cirrhosis.…”

Section: Discussionmentioning

confidence: 81%

See 1 more Smart Citation

Histopathological and Histochemical Assessment of the Protective Effects of Zinc on Ethanol-Induced Acute Hepatotoxicity in Adult Albino Rats

Elshennawy¹,

Sayed²,

Saber³

et al. 2015

J Cytol Histol

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Section: Discussionsupporting

confidence: 92%

Section: Discussionmentioning

confidence: 81%

Histopathological and Histochemical Assessment of the Protective Effects of Zinc on Ethanol-Induced Acute Hepatotoxicity in Adult Albino Rats

Elshennawy¹,

Sayed²,

Saber³

et al. 2015

J Cytol Histol

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“…Cytochrome (CY) P450 2B, 2E1 and flavin monooxygenase metabolize TAA into its toxic metabolites (30). Previous studies have identified a number of TAA-induced liver diseases, including hyperplastic liver nodules, liver cell adenomas, hepatocarcinomas, liver cirrhosis and tumors (31)(32)(33)(34)(35). In our previous study, male SD rats were administered with 300 mg/l TAA in drinking water to construct an easy and reproducible animal model recapitulating the multi-stage progression of human CCA.…”

Section: Discussionmentioning

confidence: 99%

cDNA microarray profiling of rat cholangiocarcinoma induced by thioacetamide

Yeh

Weng

Lenka

et al. 2013

Molecular Medicine Reports

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Abstract. Cholangiocarcinoma (CCA) is a malignant neoplasm affecting thousands of individuals worldwide. CCA develops through a multistep process. In the current study, an oral thioacetamide (TAA)-induced model of rat CCA was established which generates the histological progression of human CCA, particularly the mass-forming type. Seven male Sprague-Dawley rats were treated with TAA for 24 weeks to induce CCA. Following the generation of the rat CCA model, whole rat genomic oligo microarray was performed to examine gene expression profiles in CCA and non-cancerous liver samples. In brief, 10,427 genes were found to be differentially expressed (8,318 upregulated and 3,489 downregulated) in CCA compared with non-tumor liver tissue. The top 50 genes (upregulated or downregulated) were selected and their functional involvement in various pathways associated with cancer progression was analyzed, including cell proliferation, apoptosis, metabolism and the cell cycle. In addition, increased expression of CLCA3, COL1A2, DCN, GLIPr2 and NID1, and decreased expression of CYP2C7 and SLC10A1 were validated by quantitative real-time PCR. Immunohistochemical analysis was performed to determine the protein expression levels of GLIPr2 and SLC10A1. The gene expression profiling performed in this study provides a unique opportunity for understanding the carcinogenesis of TAA-induced CAA. In addition, expression profiling of a number of specific genes is likely to provide important novel biomarkers for the diagnosis of CCA and the development of novel therapeutic strategies for CCA.

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“…Prolonged administration of TAA causes hyperplastic liver nodules, liver cell adenomas and hepatocarcinomas. Various TAA induction methods have been tried in experimental animals to produce liver cirrhosis and tumors, including intraperitoneal or subcutaneous administration [7,8] and administering toxin with food [3] or drinking water [9]. TAA is known as a potent hepatotoxicant which requires metabolic activation by missed function oxidases.…”

Section: Introductionmentioning

confidence: 99%