

Author: Zhang Zuofa Jin Jie Shi Liangen
Publisher: Informa Healthcare
ISSN: 1537-6524
Source: Toxicology Mechanisms and Methods, Vol.18, Iss.8, 2008-10, pp. : 615-622
Disclaimer: Any content in publications that violate the sovereignty, the constitution or regulations of the PRC is not accepted or approved by CNPIEC.
Abstract
The hepatotoxic effects of 1,1-diphenyl-2-picryl-hydrazyl (DPPH) in ICR mice were examined. Acute liver injury was induced by a single dose of DPPH (100 mg/kg) intraperitoneally. At 12, 24, 48, and 72 h after treatment, mice were sacrificed for serum and liver. To assess hepatotoxicity, the activities of glutamate oxaloacetate transaminases (GOT), glutamate pyruvate transaminases (GPT) in serum and glutathione peroxidase (GPx), superoxide dismutase (SOD), catalase (CAT), and the levels of malonyldialdehyde (MDA), reduced glutathione (GSH), and NO in liver were measured. The present study was also conducted so that the mice which received the DPPH at doses of 25, 50, 100, 200 mg/kg, a histopathological observation and the expression of pro-inflammatory cytokines were investigated too. The result revealed that DPPH could elevate the transaminases activities and MDA and NO levels accompanied by significant reduction in GSH level and SOD, CAT, and GPx activities. The liver from the DPPH-treated mice showed prominent histopathological changes characterized by hepatocyte tumefaction and vacuolar degeneration. The mRNA levels of the pro-inflammatory cytokines were elevated in the DPPH-treated groups. The above results indicated that DPPH could induce the acute liver toxicity in mice.
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