The reported high mutagenic potency of 3-chloro-4-(dichloromethyl)-5-hydroxy-2(5H)furanone against Salmonella typhimurium (TA100) was confirmed in the determined value of 6,300 net revertantshmol. Partial inactivation of the furanone by Arochlor 1254-induced rat liver homogenate fraction (S9) was observed. Inactivation by the nucleophiles hydroxide ion, S02, S20$-, pyrrolidine and glutathione, all in aqueous solutions, was determined and the results compared. Mutagenic reduction was observed for all of the nucleophiles but was most pronounced for glutathione. Inactivation by hydroxide ion was most sensitive in the pH range of 9 to 11, was associated with chloride ion formation and paralleled irreversible ultraviolet spectral change resulting in the loss of the 227 nm absorption maximum and the appearance of a new maximum at 255 nm. Neutral aqueous solutions of the furanone and glutathione were marked by two UV maxima, at 250 and 270 nm, and lacked the aldehydic 'H-NMR signal, which was observed in the spectrum of the neutral solution of the furanone alone and was attributed to the presence of its acyclic tautomeric form. Several other furanones were prepared. Their Ames mutagenicities and those of chlorine-substituted intermediates obtained in the synthesis of the furanone were determined and compared, and then related to the reported mutagenicities of some 2-chloropropenals.

These results suggest that chicken meat is an infection source of Salmonella Infantis for humans in the Kyushu-Okinawa region, Japan. The results also showed the relatively high suitability of AFLP for application to epidemiological studies of Salmonella Infantis.

One of the mutagenic byproducts associated with chlorinated humic waters and kraft pulp bleaching effluents was recently identified as 3-chloro-4-(dichloromethyl)-5-hydroxy-2(5H)-furanone. This compound and several related chlorofuranones and precursors were synthesized and evaluated for direct-acting mutagenicity in Salmonella typhimurium tester strain TA100. Mutagenicity was greatest for 3-chloro-4-(dichloromethyl)-5-hydroxy-2(5H)-furanone, its 5-methoxy derivative, and the precursor in their synthesis, 3-(dichloromethyl)-2,4,4-trichloro-2-butenoic acid. Several of the compounds were tested in the presence of added rat liver homogenate S9 fraction, and in all cases mutagenicity was substantially reduced. An important structural feature which may govern the mutagenic response in these instances appears to be the cis arrangement of CHCl2 and Cl substituents on a carbon-carbon double bond. These compounds may also be transformed in vitro to the same acyclic chlorine substituted alpha, beta-unsaturated aldehyde derivative, which is proposed to be the agent responsible for the observed mutagenicity.