title: Acid violet 7 and its biodegradation products induce chromosome aberrations, lipid peroxidation, and cholinesterase inhibition in mouse bone marrow.
abstract: BACKGROUND
  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.
  
  
  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.
authors.affiliation: Equipe de Recherche en Physico-Chimie et Biotechnologie (ERPCB-EA3914), IUTUFR Sciences, Université de Caen Basse-Normandie, Caen, France.
authors.forename: Hédi
authors.initials: H
authors.lastname: Ben Mansour
authors.forename: Yosra
authors.initials: Y
authors.lastname: Ayed-Ajmi
authors.forename: Ridha
authors.initials: R
authors.lastname: Mosrati
authors.forename: David
authors.initials: D
authors.lastname: Corroler
authors.forename: Kamel
authors.initials: K
authors.lastname: Ghedira
authors.forename: Daniel
authors.initials: D
authors.lastname: Barillier
authors.forename: Leila
authors.initials: L
authors.lastname: Chekir-Ghedira
mesh_terms: D000083:Acetanilides / Q000633:toxicity; D000110:Acetylcholinesterase / Q000097:blood; D000332:Aerobiosis; D000818:Animals; D001391:Azo Compounds / Q000378:metabolism / Q000633:toxicity*; D001673:Biodegradation, Environmental; D001854:Bone Marrow Cells / Q000187:drug effects* / Q000378:metabolism; D002800:Cholinesterase Inhibitors / Q000378:metabolism / Q000633:toxicity*; D002869:Chromosome Aberrations / Q000139:chemically induced*; D019457:Chromosome Breakage / Q000187:drug effects; D004396:Coloring Agents / Q000378:metabolism / Q000633:toxicity*; D004305:Dose-Response Relationship, Drug; D005260:Female; D015227:Lipid Peroxidation / Q000187:drug effects*; D051379:Mice; D008807:Mice, Inbred BALB C; D009153:Mutagens / Q000633:toxicity; D009282:Naphthalenesulfonates / Q000378:metabolism / Q000633:toxicity*; D010084:Oxidation-Reduction; D016958:Pseudomonas putida / Q000378:metabolism; D011897:Random Allocation; D012303:Ring Chromosomes; D017392:Thiobarbituric Acid Reactive Substances / Q000032:analysis
chemical_list: C551248:5-acetamido-2-amino-1-hhydroxy-3,,6-naphthalenedisulfonic acid; D000083:Acetanilides; D001391:Azo Compounds; D002800:Cholinesterase Inhibitors; D004396:Coloring Agents; D009153:Mutagens; D009282:Naphthalenesulfonates; D017392:Thiobarbituric Acid Reactive Substances; D000110:Acetylcholinesterase; C519644:4-aminoacetanilide; C551247:acid violet 7