Effects of chlorophyllin on acetaldehyde: lack of modulation of the rate of sister-chromatid exchanges in mouse bone marrow, and of complex formation in aqueous solution

• Published in: Food and chemical toxicology 2002-10, Vol.40 (10), p.1507-1513
• Main Authors: Torres-Bezauri, R., Madrigal-Bujaidar, E., Alvarez-González, R.I., Zepeda, G., Chamorro, G.
• Format: Article
• Language: English
• Subjects: Acetaldehyde; Acetaldehyde - antagonists & inhibitors; Acetaldehyde - chemistry; Acetaldehyde - toxicity; Animals; Antigenotoxicity; Antimutagenic Agents - pharmacology; Biological and medical sciences; Bone Marrow - ultrastructure; Cell Division - drug effects; Chemical and industrial products toxicology. Toxic occupational diseases; Chlorophyllides - chemistry; Chlorophyllides - pharmacology; Chlorophyllin; Chromatography, High Pressure Liquid; Genotoxicity; Male; Medical sciences; Mice; Mitotic Index; Molecular complex; Mouse; Mutagens - toxicity; Sister Chromatid Exchange - drug effects; Spectrophotometry, Ultraviolet; Toxicology; Various organic compounds
• ISSN: 0278-6915; 1873-6351
• DOI: 10.1016/S0278-6915(02)00098-4

Acetaldehyde (Ace) is a reactive compound widely found in natural and industrialized products. On the other hand, chlorophyllin (Chl) is a chloropyll derivative which has shown DNA modulatory effects in several models. The first aim of the present study was to determine the capacity of Ace to increase the rate of sister-chromatid exchanges (SCEs) in mouse bone marrow cells in vivo, as well as to determine its capacity to modify the mitotic index (MI) and the average generation time (AGT). For this experiment we tested four dosages of Ace by the ip route (0.4, 4.0, 40.0 and 400 mg/kg), and found a genotoxic effect with the two highest dosages (more than double the basal level was observed with 400 mg/kg). We also found that none of the doses tested modified the MI or the AGT. A second objective was to explore the potential of Chl to modulate the genotoxicity of Ace in the same model. We evaluated whether an oral administration of Chl (2.0, 6.0 and 10.0 mg/kg), given 1 h before an ip administration of Ace (100 mg/kg), could modulate the SCEs produced by the mutagen. The result showed a similar SCE rate in both, the Ace-treated mice and those administered with the two chemicals, indicating that Chl was not a modulatory chemical on the genotoxicity of Ace. No modifications were observed concerning the MI or the AGT either. A third objective was to determine whether the two compounds (Ace and Chl) may form a molecular complex in aqueous solution. In agreement with the lack of modulatory effect by Chl, a reversed HPLC and a spectrophotometric analysis showed that the two compounds were unable to form a complex. This report confirms the importance of the specificity concerning the interaction mutagen/antimutagen.