Vanillin (3-methoxy-4-hydroxybenzaldehyde) inhibits mutation induced by hydrogen peroxide, N-methyl-N-nitrosoguanidine and mitomycin C but not (137)Cs gamma-radiation at the CD59 locus in human-hamster hybrid A(L) cells.

We have investigated the ability of the naturally occurring plant essence vanillin (3-methoxy-4-hydroxybenzaldehyde) to inhibit mutation at the CD59 locus on human chromosome 11 by hydrogen peroxide, N-methyl-N-nitrosoguanidine, mitomycin C and (137)Cs gamma-radiation in human-hamster hybrid A(L) cells. Previous studies using vanillin have suggested that it can inhibit chromosome aberrations induced by hydrogen peroxide and mitomycin C, as well as inhibiting X-ray- and UV-induced mutations at the hprt locus. Other studies with vanillin have shown that it can increase both the toxicity and mutagenicity of ethyl methane sulfonate and increase the induction of sister chromatid exchange by mitomycin C and a variety of other mutagens. The increased sensitivity of the A(L) assay, which is due in part to its ability to detect both small (single locus) and large (multilocus) genetic damage, allows us to measure the effect of vanillin at low doses of mutagen. Vanillin is shown, in these studies, to inhibit mutation induced by hydrogen peroxide, N-methyl-N-nitrosoguanidine and mitomycin C, as well as to enhance the toxicity of these agents. Vanillin had no effect on either toxicity or mutation induced by (137)Cs gamma-radiation. The vanillin-induced potentiation of H(2)O(2) toxicity is shown not to involve inhibition of catalase or glutathione peroxidase. These results show that vanillin is able to inhibit mutation at the CD59 locus and modify toxicity in a mutagen-specific manner. Possible mechanisms to explain the action of vanillin include inhibition of a DNA repair process that leads to the death of potential mutants or enhancement of DNA repair pathways that protect from mutation but create lethal DNA lesions during the repair process.

[10 years plasma exchange with the IBM (Cobe) 2997]. / Zehn Jahre Plasmaaustausch (TPA) mit der IBM (Cobe) 2997.

From 1979 to 1989 fifty patients, representing 18 different diagnoses/indications, were treated with 385 non-selective therapeutic plasma exchanges (TPE). In the first five years of the survey, the neurological diseases predominated; since 1984, these cases were treated by the Dept. of Neurology. Five % human albumin solution, fresh-frozen-plasma and saline solution were used as replacement fluids. In the beginning, the exchange volume was 1.5-2 times that of the patient's plasma volume, now it is less and varies with the disorder. ACD-A was used as anticoagulant. 11% of the TPE treatments side effects, and in another 3% technical or operator mistakes were noticed. As a supportive therapy, the plasma exchange was effective in the hyperviscosity syndrome, myasthenia gravis, thrombotic thrombocytopenic syndrome, myasthenia gravis, thrombotic thrombocytopenic purpura (TTP), hypercholesterolaemia, Guillain-Barré Syndrome, haemolytic crisis of a homozygous sickle-cell anaemia. There was, however, no definite convincing success in acute liver failure.