Desaturation of fatty acids by the psychrophilic bacterium Micrococcus cryophilus [proceedings].

l(8)-monoglucoside were non-mutagenic, as were the glucoside tetra-acetates of alizarin, chrysazin and quinizarin. When tested with the bacterial enzymes, all glucosides including the tetra-acetates were mutagenic for strain TA1537, apparently owing to formation of the free aglycones, alizarin, chrysazin, quinizarin and emodin, which are specific for strain TA11537. Emodin glucoside exhibited maximal activity after treatment with both bacterial and microsomal enzymes. Franguloside was not as clearly activated by the bacterial extracts as were the glucosides. This agent may act as some other metabolite of the parent glycone. In addition to the 0-glycosides, two anthraquinone C-glucosides, namely aloin and carminic acid, were tested by the same procedures and found to be non-mutagenic. Frameshift mutagenicity among the flavonoid compounds tested was mainly confined to the flavonols (flavon-3-01s) (Table 2). The flavonols are probably the single largest group of flavonoids, and the most mutagenic agent detected, quercetin, is the most common flavonol aglycone. Two quercetin glycones, rutin (quercetin 3-~-rutinoside) and quercitrin (quercetin 3-~-rhamnoside), were found to be very weakly mutagenic in strains TA100, TA1537 and TA98 with microsomal activation (as reported earlier by Hardigree & Epler, 1977). Mutagenic activity of the glycones for these strains could be increased 10-20-fold by incorporating gut bacterial enzymic extracts and microsomal enzymes in the assay procedure. It is still uncertain into what mutagenic intermediates the glycones are converted. Weak glycosidase activity in the S9 preparations could account for these results. A number of additional agents including four flavanone glycones (hesperidin, naringin, robinin and neoeriocitrin), 16 dihydrochalcones and three dihydrochalcone glycones (hesperetin dihydrochalcone glucoside, neohesperidin dihydrochalcone and neoeriocitrin dihydrochalcone), also were tested and found to be non-mutagenic . The implication of possible genetic toxicity of hydroxy anthraquinones is not very surprising for this group of compounds in view of other forms of toxicity exhibited by many of its members (Kean, 1968; Uraguchi et al., 1972; Wells et a[., 1975; Fairbairn, 1976). The same cannot be said for the flavonols, which, although having many physiological effects, are apparently non-toxic in man.