Protective action of an anti-oxidant (L-Ascorbic acid) against genotoxicity and cytotoxicity in mice during p-DAB-induced hepatocarcinogenesis.
BACKGROUND
DNA damage from micronutrient deficiencies has been suggested as one major cause of cancer. Therefore studies involving vitamin supplementation, particularly with those with anti-oxidant activity, in combating cancer have routinely been carried out in both in vivo and in vitro systems, but relatively much less in mice.


OBJECTIVE
The present study examines if L-Ascorbic acid (AA; vitamin C) administration has any protective abilities in combating p-DAB induced hepatocarcinogenesis in mice at cytogenetical, biochemical, histological and ultra-structural levels.


METHODS
To test if AA had a protective action against genotoxicity, cytotoxicity and tissue damage in liver during p-dimethylaminoazobenezene (p-DAB) induced hepatocarcinogenesis in mice, a group of mice were chronically fed 0.06% p-DAB and 0.05% phenobarbital (PB) for a varying period of time (7, 15, 30, 60, 90 and 120 days). A sub-group of the p-DAB plus PB fed mice were also fed 1% L-ascorbic acid. Several assays were periodically conducted (at the six intervals of fixation) for determination of genotoxic (based on chromosomal, nuclear and sperm head anomalies), cytotoxic (based on the marker enzymes aspartate transaminase; AST, alanine aminotransferase; ALT; acid phosphatase; ACP; alkaline phosphatase; ALKP; lipid peroxidation; LPO); and tissue damaging (based on optical and electron microscopic studies of liver at day 60 only) effects in these different groups of mice as compared to normal healthy control.


METHODS
Adult healthy mice of Swiss Albino strain, reared and maintained in the animal house of the Department of Zoology, Kalyani University, under supervision of Animal Welfare Committee (which oversees ethical issues), served as materials for the present study. Widely practiced standard technique has been followed for each protocol.


METHODS
The significance test between different series of data was conducted by student's t-test.


CONCLUSIONS
The results of all these studies indicated that AA had protective action against p-DAB induced hepatocarcinogenesis in mice.
Surjyo
B
B
Cytogenetics Laboratory, Department of Zoology, University of Kalyani, Kalyani-741235, West Bengal, India.
Anisur
K B
KB
D000818:Animals; D016588:Anticarcinogenic Agents / Q000627:therapeutic use; D016587:Antimutagenic Agents / Q000627:therapeutic use; D000975:Antioxidants / Q000627:therapeutic use*; D001205:Ascorbic Acid / Q000627:therapeutic use*; D002273:Carcinogens; D003602:Cytotoxicity, Immunologic / Q000187:drug effects*; D004195:Disease Models, Animal; D018757:GABA Modulators / Q000008:administration & dosage; D008099:Liver / Q000187:drug effects / Q000378:metabolism / Q000473:pathology*; D008113:Liver Neoplasms / Q000139:chemically induced / Q000517:prevention & control*; D008297:Male; D051379:Mice; D008815:Mice, Inbred Strains; D009152:Mutagenicity Tests; D010634:Phenobarbital / Q000008:administration & dosage; D013077:Sperm Head / Q000473:pathology; D013997:Time Factors; D004124:p-Dimethylaminoazobenzene
D016588:Anticarcinogenic Agents; D016587:Antimutagenic Agents; D000975:Antioxidants; D002273:Carcinogens; D018757:GABA Modulators; D004124:p-Dimethylaminoazobenzene; D001205:Ascorbic Acid; D010634:Phenobarbital