Reversible increase in the saturation of C18 fatty acids induced by diphtheria toxin in tissue culture cells

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Abstract
Diphtheria toxin (DT) reversibly increases the saturation of the long-chain C18 fatty acids (C18FA) in concentrations which are at least 100-fold smaller than the concentrations which completely inhibit host cell protein synthesis. The concentrations required for induction of the increase in the saturation of the C18FA in fibroblasts are 100-fold smaller than the concentrations for the epithelial cells. The increase in saturation of the C18FA was proportional to the concentration of DT. A cytopathic effect appeared with DT concentrations which induced a near-maixmal increase in the saturation of the C18FA, but the cells remained viable. At very high concentrations of DT and depending on the type of cell, there was no change in the fatty acids, and the treated cells disintegrated. Interferon, which also induces a reversible increase in the saturation of the C18FA, produces a cumulative effect when used in conjunction with DT. This additive effect of DT and interferon is discussed in the light of other similar biological activities of these agents. [Bovine kidney PBKC, rabbit kidney RK-13, chicken embryo fibroblast and human fibroblast MRC5 cells were used in this study.].