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.

Adhesion of Erysipelothrix rhusiopathiae to cultured rat aortic endothelial cells. Role of bacterial neuraminidase in the induction of arteritis.

The adhesion of Erysipelothrix rhusiopathiae (E. rhusiopathiae) to the cultured confluent monolayer of rat aortic endothelial cells (EC) and the role of neuraminidase in the interaction between EC and E. rhusiopathiae were examined. One EC line was obtained by collagenase treatment of rat aorta. The EC showed a typical cobblestone appearance and possessed the factor VIII related antigen. When cultured more than two weeks after reaching confluence, the EC formed a vascular plexus-like appearance. E. rhusiopathiae began to adhere to EC within 2 minutes after the beginning of culture and adhered at a constant rate for 20 minutes. The adhesion of bacteria to EC was closely related to the release of sialic acid from the EC. Significantly more bacteria adhered to neuraminidase treated EC, and bacterial adhesion was inhibited dose-dependently by N-acetylneuraminic-lactose, which is the substrate of bacterial neuraminidase. It is concluded that bacterial neuraminidase plays an essential role in initiating the interaction between EC and E. rhusiopathiae, which would contribute to the genesis of arteritis.

Light microscopic investigations on lysozyme- and penicillin-induced morphological changes in Erysipelothrix rhusiopathiae and on propagation of its protoplast type L-form.

Although lysozyme and penicillin are different in their molecular action on cell wall murein they produce similar morphological changes in Erysipelothrix rhusiopathiae grown on agar media. 2,000--5,000 micrograms/ml lysozyme and 0.1--2 IU/ml penicillin induce filament formation. Filaments are able to divide in rods, which shows that only cross wall formation and separation are inhibited. Higher doses of lysozyme (10,000 micrograms/ml) and penicillin (less than 1 IU/ml) inhibit cell wall synthesis and induce L-form growth. The propagation of this protoplast type L-form was investigated by microphotographic series in phase contrast microscope during L-form induction and in the stable L-form state. In both cases L-form cells propagate by formation and growth of small granular elements of about 0.2--0.6 micrometers in diameter, which spread in different directions in the agar medium. The multiplication process may be explained by the plasticity and flexibility of the L-form cell and its cytoplasmic membrane and by the structural and functional interaction between the "folded chromosome" and the surrounding cytoplasm.

L-form induction, morphology, and development in two related strains of Erysipelothrix rhusiopathiae.

Two related strains of Erysipelothrix rhusiopathiae, one the parent and the other an L-form revertant, were studied for their propensity or ability to produce L-forms under the influence of penicillin. The parent strain produced L-forms in nutrient solid media in an osmolarity range between 0.85 and 5.0% NaCl concentration whereas the revertant strain did so between 0.5 and 3.0% NaCl concentration. When various hyperosmolar media were tried without penicillin, recovery of L-forms from the revertant strain was optimal at a salt concentration of 2.0%, whereas the parent strain occasionally produced a few L-forms on 3.0% salt medium only. The process of penicillin-induced transformation from bacteria to L-form followed an unusual morphological sequence, beginning with beading of the bacterial body, followed by disintegration into granules from which the L-form colony derived. No large bodies were seen during the initial process of L-form induction, but they evolved later from the original granules and had the potential to reproduce L-type growth. The spontaneous development of L-forms in hyperosmolar media had a different morphological sequence starting with elongation of the bacteria into filaments which later developed polar and central dilatations from which granules and L-type growth developed. The differences in biological behavior between these related bacterial strains suggest that the revertant strain developed new properties, probably of genetic origin. Consequently, the assumption that L-forms revert to the "parent" bacteria may not always be justified. It can be made only after the biological properties of the parent and the revertant organisms have been properly identified.