human
The task is to decide the Hallmarks of Cancer (HOC) taxonomy of the article based on its abstract. The input is an abstract text. There are 10 topics you will need to decide whether the article is related to. Topics: sustaining proliferative signaling, evading growth suppressors, resisting cell death, enabling replicative immortality, inducing angiogenesis, activating invasion and metastasis, genomic instability and mutation, tumor promoting inflammation, cellular energetics, avoiding immune destruction. The output should be topics from the above 10 topics, that are related to the input article. Please note one article can be related to multiple topics. Output format: provide a semicolon-separated list of relevant topics.
    ###
    INPUT: OBJECTIVES Toxicity caused by pharmacological and chemical substances , including carbon tetrachloride ( CCl(4) ) , is a major pathological factor for liver injury . Therefore , strategies to prevent toxicity are needed for maintaining a healthy liver . This study was designed to determine whether recombinant bovine pancreatic trypsin inhibitor ( rBPTI ) , a non-specific serine protease inhibitor , prevents CCl(4)-induced liver injury in mice . METHODS Mice were treated with CCl(4) in the presence or absence of co-treatment with rBPTI . Liver sections were prepared for histopathological assessment . Liver function was evaluated by detecting serum levels of alanine aminotransferase ( ALT ) and aspartate aminotransferase ( AST ) and liver index . Liver oxidative stress and inflammation were examined by detecting the liver malondialdehyde level and glutathione and superoxide dismutase activity , and serum tumour necrosis factor-alpha level , respectively . KEY FINDINGS CCl(4) induced hepatocyte necrosis , inflammatory cell infiltration and fatty degeneration , which were ameliorated by co-treatment with rBPTI in a concentration-dependent manner . Furthermore , rBPTI prevented CCl(4)-induced disruption of liver function . Importantly , rBPTI reduced CCl(4)-induced liver oxidative stress response and pro-inflammatory cytokine production . CONCLUSIONS These results indicated that rBPTI exerted a protective effect on CCl(4)-induced liver injury in mice . Thus , rBPTI may have potential application for prevention of liver injury induced by metabolism of drugs and toxic substances .
    OUTPUT:

agent
resisting cell death;tumor promoting inflammation
The task is to decide the Hallmarks of Cancer (HOC) taxonomy of the article based on its abstract. The input is an abstract text. There are 10 topics you will need to decide whether the article is related to. Topics: sustaining proliferative signaling, evading growth suppressors, resisting cell death, enabling replicative immortality, inducing angiogenesis, activating invasion and metastasis, genomic instability and mutation, tumor promoting inflammation, cellular energetics, avoiding immune destruction. The output should be topics from the above 10 topics, that are related to the input article. Please note one article can be related to multiple topics. Output format: provide a semicolon-separated list of relevant topics.
    ###
    INPUT: OBJECTIVES Toxicity caused by pharmacological and chemical substances , including carbon tetrachloride ( CCl(4) ) , is a major pathological factor for liver injury . Therefore , strategies to prevent toxicity are needed for maintaining a healthy liver . This study was designed to determine whether recombinant bovine pancreatic trypsin inhibitor ( rBPTI ) , a non-specific serine protease inhibitor , prevents CCl(4)-induced liver injury in mice . METHODS Mice were treated with CCl(4) in the presence or absence of co-treatment with rBPTI . Liver sections were prepared for histopathological assessment . Liver function was evaluated by detecting serum levels of alanine aminotransferase ( ALT ) and aspartate aminotransferase ( AST ) and liver index . Liver oxidative stress and inflammation were examined by detecting the liver malondialdehyde level and glutathione and superoxide dismutase activity , and serum tumour necrosis factor-alpha level , respectively . KEY FINDINGS CCl(4) induced hepatocyte necrosis , inflammatory cell infiltration and fatty degeneration , which were ameliorated by co-treatment with rBPTI in a concentration-dependent manner . Furthermore , rBPTI prevented CCl(4)-induced disruption of liver function . Importantly , rBPTI reduced CCl(4)-induced liver oxidative stress response and pro-inflammatory cytokine production . CONCLUSIONS These results indicated that rBPTI exerted a protective effect on CCl(4)-induced liver injury in mice . Thus , rBPTI may have potential application for prevention of liver injury induced by metabolism of drugs and toxic substances .
    OUTPUT:
