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Citral inhibits N‐nitrosodiethylamine‐induced hepatocellular carcinoma via modulation of antioxidants and xenobiotic‐metabolizing enzymes
Author(s) -
Krishnan Palanisamy,
Sundaram Jagan,
Salam Sharmila,
Subramaniam Nirmala,
Mari Ashok,
Balaraman Gopalakrishnan,
Thiruvengadam Devaki
Publication year - 2020
Publication title -
environmental toxicology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.813
H-Index - 77
eISSN - 1522-7278
pISSN - 1520-4081
DOI - 10.1002/tox.22933
Subject(s) - citral , hepatocellular carcinoma , enzyme , pharmacology , chemistry , xenobiotic , biochemistry , carcinogenesis , cancer research , biology , essential oil , chromatography , gene
Hepatocellular carcinoma (HCC) ranks the sixth position among various cancers worldwide. Recent research shows that natural and dietary compounds possess many therapeutic effects. Citral is a monoterpene aldehyde that contains geranial and neral. The present study was considered to study the role of citral against N‐nitrosodiethylamine (NDEA)‐induced HCC via modulation of antioxidants and xenobiotic‐metabolizing enzymes in vivo. NDEA‐alone‐administered group II animals profoundly showed increased tumor incidence, reactive oxygen species, liver marker enzyme levels, serum bilirubin levels, tumor markers of carcinoembryonic antigen, α‐fetoprotein, proliferative markers of argyrophilic nucleolar organizing regions, proliferating cell nuclear antigen (PCNA) expressions, phase I xenobiotic‐metabolic enzymes and simultaneously decreased antioxidants, and phase II enzymes levels. Citral (100 mg/kg b.w.) treatment significantly reverted the levels in group III cancer‐bearing animals when compared to group II cancer‐bearing animals. In group IV animals, citral‐alone administration did not produce any adverse effect during the experimental condition. Based on the results, citral significantly inhibits the hepatocellular carcinogenesis through restoring the antioxidants and phase II xenobiotic‐enzyme levels; thereby, it strongly proves as an antiproliferative agent against rat HCC.