Assessment of the carcinogenicity associated with oral exposures to hydrogen peroxide

Citation
Jm. Desesso et al., Assessment of the carcinogenicity associated with oral exposures to hydrogen peroxide, FOOD CHEM T, 38(11), 2000, pp. 1021-1041
Citations number
83
Categorie Soggetti
Food Science/Nutrition","Pharmacology & Toxicology
Journal title
FOOD AND CHEMICAL TOXICOLOGY
ISSN journal
02786915 → ACNP
Volume
38
Issue
11
Year of publication
2000
Pages
1021 - 1041
Database
ISI
SICI code
0278-6915(200011)38:11<1021:AOTCAW>2.0.ZU;2-Y
Abstract
Concern regarding hydrogen peroxide (H2O2) carcinogenicity arises from its ability to act as a strong oxidizing agent. In short-term genotoxicity test s, H2O2 has given predominantly positive results; however, these assays hav e been performed using either bacterial strains engineered to be exquisitel y sensitive to oxidant damage, or mammalian cells deficient in antioxidant enzymes. Significantly, the addition of antioxidant protective measures (no rmally present in vivo) to these assay systems protects against H2O2 genoto xicity. In most whole animal studies, H2O2 exposure neither initiates nor p romotes tumors. In mice, however, 0.4% H2O2 in drinking water was reported to induce hyperplastic lesions of the duodenum and to erode areas in the gl andular stomach epithelium. Owing to the chemistry of dilute H2O2 solutions and the anatomy/physiology of the gastrointestinal tract, it is unlikely t hat orally ingested H2O2 reaches the duodenum. Instead, greatly decreased w ater consumption and the resultant abrasion of the luminal lining on ingest ion of pelleted dry rodent chow is the most likely cause of the observed ga stric and duodenal lesions following H2O2 administration in drinking water. Significantly, when hamsters received high doses of H2O2 by gastric intuba tion (and water intake was not affected), the gastric and duodenal epitheli a appeared normal. In-depth analysis of the available data supports the con clusion that oral ingestion of H2O2 should not be considered a carcinogenic threat. (C) 2000 Elsevier Science Ltd. All rights reserved.