Effects of tamoxifen, melatonin, coenzyme Q10, and L-carnitine supplementation on bacterial growth in the presence of mycotoxins.
The involvement of toxic oxygen intermediates in the bacteriostatic effects of mycotoxins (T-2 toxin, deoxynivalenol, ochratoxin A, aflatoxin B1, and fumonisin B1) was investigated by producing bacterial growth curves using turbidimetry assays in the presence and absence of oxygen radical-scavenging substances. The strains used in this study included Escherichia coli (FT 101), Streptococcus agalactiae (FT 311, FT 313, FT 315), Staphylococcus aureus (FT 192), Yersinia enterocolitica (FT 430), Salmonella infantis (FT 431), Erysipelothrix rhusiopathiae (FT 432), Lactobacillus plantarum (FT234) and Lactobacillus casei (FT 232). Tamoxifen, melatonin, l-carnitine and coenzyme Q10 were used as radical scavengers against oxygen toxicity to the strains studied. Tamoxifen was the most effective in inhibiting bacterial growth when used at a high concentration, whereas melatonin and l-carnitine were less effective. A combination of l-carnitine and coenzyme Q10 provided better protection against oxygen toxicity caused by the mycotoxins growth than they did individually. It was concluded that oxygen radicals are involved in the killing of bacteria and that there is endogenous formation of toxic oxygen products by mycotoxins. The objective of this study was to determine whether the antioxidants were able to counteract the toxic effects of the mycotoxins. The data obtained indicate that bacterial growth can be inhibited especially by T-2 toxin, aflatoxin B1 and ochratoxin A and that this effect can be partially counteracted by antioxidants such as coenzyme Q10 plus l-carnitine.
Department of Clinical Sciences, Faculty of Veterinary Medicine, University of Helsinki, Helsinki, Finland.
F
F
Atroshi
A
A
Rizzo
T
T
Westermarck
T
T
Ali-vehmas
D016604:Aflatoxin B1 / Q000633:toxicity; D018931:Antineoplastic Agents, Hormonal / Q000494:pharmacology*; D000975:Antioxidants / Q000494:pharmacology*; D001419:Bacteria / Q000166:cytology* / Q000187:drug effects*; D002264:Carboxylic Acids / Q000633:toxicity; D002331:Carnitine / Q000494:pharmacology; D002455:Cell Division / Q000187:drug effects; D003067:Coenzymes; D004305:Dose-Response Relationship, Drug; D004888:Erysipelothrix / Q000166:cytology / Q000187:drug effects; D004926:Escherichia coli / Q000166:cytology / Q000187:drug effects; D037341:Fumonisins; D007778:Lactobacillus / Q000166:cytology / Q000187:drug effects; D007780:Lacticaseibacillus casei / Q000166:cytology / Q000187:drug effects; D008550:Melatonin / Q000494:pharmacology; D009183:Mycotoxins / Q000633:toxicity*; D009793:Ochratoxins / Q000633:toxicity; D012475:Salmonella / Q000166:cytology / Q000187:drug effects; D013211:Staphylococcus aureus / Q000166:cytology / Q000187:drug effects; D013292:Streptococcus agalactiae / Q000166:cytology / Q000187:drug effects; D013605:T-2 Toxin / Q000633:toxicity; D013629:Tamoxifen / Q000494:pharmacology*; D014255:Trichothecenes / Q000633:toxicity; D014451:Ubiquinone / Q000031:analogs & derivatives / Q000494:pharmacology; D015008:Yersinia enterocolitica / Q000166:cytology / Q000187:drug effects
D018931:Antineoplastic Agents, Hormonal; D000975:Antioxidants; D002264:Carboxylic Acids; D003067:Coenzymes; D037341:Fumonisins; D009183:Mycotoxins; D009793:Ochratoxins; D014255:Trichothecenes; D013629:Tamoxifen; D014451:Ubiquinone; C025589:ochratoxin A; C056933:fumonisin B1; D016604:Aflatoxin B1; C024989:coenzyme Q10; D013605:T-2 Toxin; D008550:Melatonin; C007262:deoxynivalenol; D002331:Carnitine