Proanthocyanidin exposure to B6C3F1 mice significantly attenuates dimethylnitrosamine-induced liver tumor induction and mortality by differentially modulating programmed and unprogrammed cell deaths

Mutation Research - Fundamental and Molecular Mechanisms of Mutagenesis

Volumn 579, Issue 1-2, 2005, Pages 81-106

  Ray, Sidhartha D ^a,b   Parikh, Hemal ^a   Bagchi, Debasis ^a,b  

^a LONG ISLAND UNIVERSITY   (United States)

^b CREIGHTON UNIVERSITY MEDICAL CENTER   (United States)

Author keywords

Apoptosis; DMN; DNA damage; Grape seed proanthocyanidins; Hepatocarcinogenesis; Mice; Prevention

Indexed keywords

DIMETHYLNITROSAMINE; GENOMIC DNA; PROANTHOCYANIDIN;

ANIMAL MODEL; ANIMAL TISSUE; ANTIOXIDANT ACTIVITY; APOPTOSIS; ATTENUATION; BODY WEIGHT; CONFERENCE PAPER; CONTROLLED STUDY; GRAPEFRUIT; HISTOPATHOLOGY; LETHALITY; LIVER CARCINOGENESIS; MALE; METABOLISM; MORTALITY; MOUSE; NONHUMAN; OXIDATIVE STRESS; PRIORITY JOURNAL;

ANIMALS; ANTIOXIDANTS; APOPTOSIS; CELL DEATH; CREATINE KINASE; DIMETHYLNITROSAMINE; GLUTATHIONE; KIDNEY; LIPID PEROXIDES; LIVER; LIVER NEOPLASMS; MALE; MICE; MICE, INBRED STRAINS; PLANT EXTRACTS; PROANTHOCYANIDINS; SUPEROXIDE DISMUTASE;

ANIMALIA; CITRUS X PARADISI; VITIS SP.;

EID: 27544500250     PISSN: 00275107     EISSN: None     Source Type: Journal    
DOI: 10.1016/j.mrfmmm.2005.02.017     Document Type: Conference Paper

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