Modification of diamine oxidase activity in vitro by metabolites of asparagine and differences in asparagine decarboxylation in normal and virus-transformed baby hamster kidney cells

The oxidation of putrescine in vitro by pig kidney diamine oxidase (EC 1.4.3.6) was increased in the presence of 2-oxosuccinamic acid and malonamic acid. It was inhibited by 3-aminopropionamide, oxaloacetate and pyruvate. 2-Oxosuccinamate was derived from asparagine in virus-transformed baby hamster kidney (BHK) cells growing in tissue culture. Asparagine was decarboxylated more efficiently by transformed than by normal BHK cells. In BHK cells transformed by polyoma virus (Py BHK), 2-oxosuccinamate is the most likely immediate precursor of the 14 CO2 arising from [U-14C] asparagine, and there was some evidence for its formation in an asparagine-dependent clone of BHK cells before and after their transformation by hamster sarcoma virus (respectivey Asn- and HSV Asn-). The relationship between 2-oxosuccinamate and pyruvate and the possible roles of these two substances in controlling cellular diamine oxidase activity are discussed (AU)

Identification of ethylmalonic acid in urine of two patients with the vomiting sickness of Jamaica

Large amounts of ethylmalonic acid have been identified in urines from two patients with the vomiting sickness of Jamaica. The amounts were 178 and 882æg per mg creatinine which are 70 and 350 times, respectively, over control values. Other short and medium chain dicarboxylic acids including glutaric and adipic acids and those with eight and ten carbon chain, saturated and cis-unsaturated, were also detected in large quantities as in the case of hypoglycin treated rats' urine. However, the large increase of urinary ethylmalonic acid in these two human cases is in a sharp contrast to the findings in hypoglycin treated rats in which urinary ethylmalonic acid increased only 3 times over control. It appears that ethylmalonic acid is produced in the cases with the vomiting sickness of Jamaica by carboxylation of n-butyryl-CoA which is not oxidised further due to the inhibition by hypoglycin A. In case of hypoglycin-treated rats, n-butyryl-CoA is mainly conjugated with glycine or deacylated to free butyric acid.(Summary)

Serum Beta-aminopropionaldehyde: identification and origin

Beta-aminopropionaldehyde is one of the serum aldehydes whose level increases on treating serum with As2O3 and methanol. In animal tissues, beta-aminopropionaldehyde can arise directly from the oxidation of spermidine or diaminopropane. A pathway linking spermidine, b-aminopropionaldehyde and malondialdehyde to the control of RNA and DNA synthesis is proposed (AU)