Adeninephosphoribosyltransferase (APRT)-activity in patients with nephrolithiasis or renal failure.
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Biomedical subjects
Publications and source records attributed to N Zöllner.
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Abdominal ultrasonic screening of patients clinically asymptomatic of abdominal disease was performed in 5 720 subjects. In these asymptomatic persons pathological ultrasonic findings were reported in 47.1% of all cases, but these were mostly without clinical relevance. This is especially true for diffuse liver disease (30.9%), asymptomatic gallstones (6.1%), and typical renal cysts (5.7%). Asymptomatic malignant abdominal tumours (0.2% or 13 cases) were detected very rarely, and were found to be mostly renal carcinomas.
2-Acetyl-S-octadecyl-rac-1-thioglycero-3-phosphocholine, the thio analog of platelet-activating factor, in concentrations of 10(-6) M to 10(-12) M in the medium, lowers cAMP-concentrations in rat hepatocytes. In a concentration of 10(-4) M, the thio analog aggregates human platelets irreversibly, above 10(-5) M aggregation shows a reversible course. Compared with the saturated or unsaturated ether analogs, the thio compound shows less platelet-aggregating potency. We have correlated this difference in platelet aggregation with reduced cAMP-depressing activity of the thio analog (compared with saturated and unsaturated 2-acetyl-1-O-alkyl-sn-glycero-3-phosphocholines).
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Young healthy volunteers received a purine-free, isoenergetic formula diet over a period of 28 to 32 days. After a short time under formula diet alone 400 mg allopurinol were administered daily. After a further 10 days each volunteer received daily, in addition, either 4 g RNA, 4 g RNA-hydrolysate, 1 g guanosine-5-monophosphate (GMP), 1 or 3 g adenosine-5-monophosphate (AMP), uridine-5-monophosphate (UMP), cytidine-5-monophosphate (CMP) or adenosine, guanosine, uridine, cytidine, guanine, hypoxanthine, xanthine, cytosine and uracil. Finally the allopurinol was omitted. The renal excretion of total orotic acid (orotic acid and orotidine), uric acid and creatinine was determined daily; serum uric acid concentrations and the enzyme activities of orotidine-5-phosphate-decarboxylase (ODCase) and hypoxanthine-guanine-phosphoribosyltransferase (HGPRTase) from erythrocytes were determined every other day. The results show that RNA, RNA-hydrolysate, purine- and pyrimidine-nucleotides and -nucleotides as well as hypoxanthine, and to a lesser extent adenine, diminish allopurinol-induced orotaciduria. This is compatible with an influence of dietary purines and pyrimidines on human pyrimidine biosynthesis.
Among 64 patients with familial hypercholesterolemia (FHC) confirmed by tissue culture of skin fibroblasts (3 homozygotes, 9 heterozygotes) 12 (3 homozygotes, 9 heterozygotes) had signs of atherosclerosis of the carotid arteries and of the peripheral arteries (extracardiac vasculature). 8 heterozygotes as well as the three homozygotes had coronary atherosclerosis. Three of the 12 patients with carotid artery disease suffered from clinical symptoms of cerebrovascular insufficiency. Only five patients with heterozygous FHC had symptomatic peripheral artery disease though 10 including the three homozygotes had signs of atherosclerosis of the abdominal aorta and its peripheral branches. It is concluded that patients with FHC develop generalized atherosclerosis but not always symptoms of peripheral artery disease. Risk factors other than hypercholesterolemia do not seem to contribute essentially to the development of atherosclerosis. It seems important to evaluate patients with FHC regularly for atherosclerosis of the carotid arteries which might be recognized earlier than coronary atherosclerosis.
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The hormonal regulation of two regulatory enzymes of fatty acid synthesis acetyl-CoA carboxylase (EC 6.4.1.2) and glucose-6-phosphate dehydrogenase (EC 1.1.1.49), has been investigated in human diploid fibroblasts. There was a 35% increase in acetyl-CoA carboxylase activity, 72 h following addition of 10 microU/ml insulin to the culture medium. Addition of 1 microgram/ml of 3,3'5-triiodothyronine for 72 h resulted in an increase in acetyl-CoA carboxylase activity to 166% of the controls. The simultaneous addition of 1 microgram/ml triiodothyronine and 10 mU/ml insulin caused the enzyme activity to rise to 240% of the controls. A dose-dependent reduction in acetyl-CoA carboxylase activity was brought about by 1 X 10(-4) to 1 X 10(-3) M dibutyryl cyclic AMP. The earliest effect of dibutyryl cyclic AMP was observed within 24 h. Glucose-6-phosphate dehydrogenase followed qualitatively the same pattern of response, whereas the constitutive enzyme, lactate dehydrogenase (EC 1.1.1.27), did not show significant changes in these experiments. The data demonstrate common features of hormonal regulation of lipogenesis in human fibroblasts with liver and adipose tissue and substantiate the growing evidence that thyroid hormones are of major importance for the regulation of this process.
1-0-Alkyl-2-0-acetoyl-sn-glycero-3-phosphocholines, containing saturated or unsaturated alkyl moieties and their 2-lyso derivatives, prepared from ratfish liver oil (Hydrolagus colliei), were studied for their in vitro effect on cellular adenosine 3':5'-cyclic monophosphate (cAMP) concentration in freshly isolated hepatocytes from adult rats. We report here for the first time that semisynthetic platelet-activating factor (PAF), the saturated and unsaturated compound, from 10(-6) M to 10(-12) M, is effective in lowering cAMP concentrations by 50% after 4 h of incubation. This effect becomes apparent after 30 min. Concentrations from 10(-12) M up to 10(-20) M did not influence cAMP levels. The 2-lyso derivatives (10(-8) M) of both compounds are equally active as compared to their 2-0-acetoyl derivatives, in lowering cAMP levels after 4 h of incubation. We discuss the existence of a transacetylating enzyme, generating the active form in rat liver cells.
1-O-Alkyl-2-O-acetyl-sn-glycero-3-phosphocholines (platelet activating factor, PAF) aggregate human thrombocytes in a concentration dependent fashion. After a short lag-phase, maximum aggregation is reached within 2 min. PAF releases serotonin from human thrombocytes within 1 min. Indomethacin and creatine phosphate (CP)/creatine phosphokinase (CPK) are able to inhibit the second phase of the aggregation by PAF, while xylocain reduces both the first and second phase of aggregation of human thrombocytes. Hirudine neither influences the first nor the second phase of aggregation by PAF.
Twenty-three patients with familial hypercholesterolemia (FHC) confirmed by tissue cultures of skin fibroblasts (2 homozygotes, 21 heterozygotes) and 3 patients with sporadic hypercholesterolemia were evaluated for Achilles tendon (AT) thickness by xeroradiography. Both homozygotes had thick ATs and coronary heart disease (CHD), 20 heterozygotes had thick ATs, but only 8 of them had CHD. One heterozygote had a small AT value, but CHD for a long time. The 3 patients with sporadic hypercholesterolemia, one with CHD, had small AT. There was no correlation between serum cholesterol concentration and AT thickness, between age and AT thickness, nor between AT thickness and CHD.