{"doi":"10.17615/jxh6-nt58","title":"Acetaminophen-induced acute liver injury in HCV transgenic mice","abstract":"The exact etiology of clinical cases of acute liver failure is difficult to ascertain and it is likely that various co-morbidity factors play a role. For example, epidemiological evidence suggests that coexistent hepatitis C virus (HCV) infection increased the risk of acetaminophen-induced acute liver injury, and was associated with an increased risk of progression to acute liver failure. However, little is known about possible mechanisms of enhanced acetaminophen hepatotoxicity in HCV-infected subjects. In this study, we tested a hypothesis that HCV-Tg mice may be more susceptible to acetaminophen hepatotoxicity, and also evaluated the mechanisms of acetaminophen-induced liver damage in wild type and HCV-Tg mice expressing core, E1 and E2 proteins. Male mice were treated with a single dose of acetaminophen (300 or 500 mg/kg in fed animals; or 200 mg/kg in fasted animals; i.g.) and liver and serum endpoints were evaluated at 4 and 24 hrs after dosing. Our results suggest that in fed mice, liver toxicity in HCV-Tg mice is not markedly exaggerated as compared to the wild-type mice. In fasted mice, greater liver injury was observed in HCV-Tg mice. In fed mice dosed with 300 mg/kg acetaminophen, we observed that liver mitochondria in HCV-Tg mice exhibited signs of dysfunction showing the potential mechanism for increased susceptibility.","journal":"UNC Libraries","year":2020,"id":117276,"datarank":0.0,"base_score":0.0,"endowment":0.0,"self_citation_contribution":0.0,"citation_network_contribution":0.0,"self_endowment_contribution":0.0,"citer_contribution":0.0,"corpus_percentile":null,"corpus_rank":null,"citation_count":1,"citer_count":0,"citers_with_citation_signal":0,"citers_with_endowment":0,"datacite_reuse_total":0,"is_dataset":false,"is_dataset_confidence":0.9504,"is_data_producer":false,"deposit_databanks":null,"is_oa":true,"file_count":0,"downloads":0,"has_version_chain":false,"published_date":"2020-01-01","fair_score":null,"fair_percentile":null,"algorithm_id":"datarank_citation_only_1hop_v6","ranking_scope":"data_only","authors":[{"id":547532,"name":"Gary A. Boorman","orcid":null,"position":1,"is_corresponding":false},{"id":299483,"name":"Ivan Rusyn","orcid":"0000-0001-9340-7384","position":2,"is_corresponding":false},{"id":476851,"name":"Volodymyr Tryndyak","orcid":"0000-0002-8319-2954","position":3,"is_corresponding":false},{"id":453064,"name":"Igor P. Pogribny","orcid":"0000-0002-5248-9843","position":4,"is_corresponding":false},{"id":230908,"name":"Saurabh Chatterjee","orcid":"0000-0003-1649-7149","position":5,"is_corresponding":false},{"id":547533,"name":"Blair U. Bradford","orcid":null,"position":6,"is_corresponding":false},{"id":524572,"name":"Jeffrey M. Macdonald","orcid":null,"position":7,"is_corresponding":false},{"id":546836,"name":"Takeki Uehara","orcid":"0000-0002-5853-9426","position":8,"is_corresponding":false},{"id":524571,"name":"Katherine Tech","orcid":null,"position":9,"is_corresponding":false},{"id":546837,"name":"Ronald P. Mason","orcid":"0000-0002-1859-9109","position":10,"is_corresponding":false},{"id":88320,"name":"Emmanuelle Jeannot","orcid":"0000-0002-4851-7450","position":11,"is_corresponding":false},{"id":303876,"name":"Oksana Kosyk","orcid":"0000-0003-0873-3180","position":12,"is_corresponding":false},{"id":357190,"name":"Stepan B. Melnyk","orcid":null,"position":0,"is_corresponding":true}],"reference_count":0,"raw_metadata":null,"created_at":"2026-07-18T23:13:51.309289Z","pmid":null,"pmcid":null,"fwci":null,"citation_percentile":null,"influential_citations":0,"oa_status":null,"license":null,"views":0,"total_file_size_bytes":0,"version_count":0,"fair_f":null,"fair_a":null,"fair_i":null,"fair_r":null,"fair_zscore":null,"fair_rationale":null,"fair_model":null,"fair_agent_version":null,"fair_fulltext_source":null,"fair_has_llm":null,"fair_computed_at":null,"clinical_trials":[],"software_tools":[],"db_accessions":[],"linked_datasets":[],"topics":[]}