Abstract Title:

Acid violet 7 and its biodegradation products induce chromosome aberrations, lipid peroxidation, and cholinesterase inhibition in mouse bone marrow.

Abstract Source:

Environ Sci Pollut Res Int. 2010 Aug;17(7):1371-8. Epub 2010 Apr 6. PMID: 20369386

Abstract Author(s):

Hédi Ben Mansour, Yosra Ayed-Ajmi, Ridha Mosrati, David Corroler, Kamel Ghedira, Daniel Barillier, Leila Chekir-Ghedira

Article Affiliation:

Equipe de Recherche en Physico-Chimie et Biotechnologie (ERPCB-EA3914), IUTUFR Sciences, Université de Caen Basse-Normandie, Caen, France.


INTRODUCTION: Acid violet 7 (AV7), mostly used in food, paper, cosmetic, and especially in textile industries, was degraded by Pseudomonas putida mt-2 at concentrations up to 200 mg/l. MATERIALS AND METHODS: In this study, toxicity of AV7, before and after biodegradation, was evaluated in vivo, in mouse bone marrow, by assessing the percentage of cells bearing different chromosome aberrations, membrane lipid peroxidation, and acetylcholinesterasic activity inhibition. The studies included same conditions for animal treatment, corresponding to increasing doses by intraperitoneal (ip) injection. RESULTS: Results indicated that AV7 showed a significant ability to induce chromosome aberrations, lipid peroxidation, and acetylcholinesterase inhibitory effect. The toxicity of AV7 increased significantly after static biodegradation with P. putida mt-2 and totally disappeared after shaken incubation. In addition, the toxicity generated by the pure azo dye and the corresponding azoreduction metabolites (4'-aminoacetanilide (4'-AA) and 5-acetamido-2-amino-1-hydroxy-3,6-naphtalene disulfonic acid (5-ANDS)) were compared. 4'-AA and 5-ANDS would be responsible of static biodegradation medium toxicity. The present study demonstrates that P. putida mt-2, incubated under aerobic condition, has a catabolism which enables it to degrade AV7, and especially to completely detoxify the dye mixture.

Study Type : Animal Study
Additional Links
Problem Substances : Acid Violet : CK(2) : AC(1)

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