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PubMed1989

Contraluminal para-aminohippurate (PAH) transport in the proximal tubule of the rat kidney. VI. Specificity: amino acids, their N-methyl-, N-acetyl- and N-benzoylderivatives; glutathione- and cysteine conjugates, di- and oligopeptides.

In order to evaluate the specificity of the renal contraluminal PAH transport system for amino acids, oligopeptides and their conjugates, the inhibitory potency of these substances against contraluminal [3H] PAH influx has been determined. For this, inhibition of 3H-PAH flux from the interstitium into cortical tubular cells of the rat kidney in situ has been measured. Apparent Ki values were evaluated by a computer program assuming competitive inhibition. Unconjugated amino acids (glycine, cysteine, alanine, leucine, phenylalanine, tyrosine, aspartate, glutamate, arginine, ornithine and lysine) do not inhibit [3H] PAH influx. The very hydrophobic tryptophan, however, does. N-alpha-methylation does not change this behaviour. N-alpha-acetylation does not evoke interaction with the PAH transporter when it occurs with glycine, cysteine (to yield mercapturic acid), arginine, ornithine and lysine. However, it renders alanine, leucine, phenylalanine, tryptophan, L-aspartate moderately, and L-glutamate strongly, inhibitory. The acetylated D-isomers of alanine, leucine and phenylalanine exert a higher inhibitory potency compared with the respective L-isomers. N-alpha-benzoylation of L-lysine is ineffective. N-alpha-benzoylation, however, evokes interaction with the PAH transporter, when it occurs with ornithine less than arginine less than histidine less than glycine = leucine less than alanine = phenylalanine = aspartate = glutamate. Dipeptides interact with the PAH transporter according to their hydrophobicity (Nozaki scale down to 0.9, Fauchère scale up to 1.0). N-acetylation does not change this behaviour. Hydrophobicity also renders oligopeptides, as angiotensin II, inhibitory against PAH transport. Similarly the anionic angiotensin I converting enzyme inhibitors Captopril, Enalapril and Ramipril inhibit contraluminal PAH influx.

Acetylation↗
PubMed1997

Toxic effect of concomitant administration of cyclosporin A and acyclovir on renal function and morphology in rats.

The immunosuppressive agent cyclosporin A (CyA) and the antiviral drug acyclovir may cause renal functional impairment. CyA-induced immunosuppression increases the rate of viral infections. Therefore we were interested to determine whether short-term co-administration of CyA and acyclovir involves an increased nephrotoxic risk. Male Wistar rats were treated with CyA (20 mg/kg body wt., s.c., once daily for 8 days), acyclovir (15 mg/kg body wt., s.c., 3-times daily for the last 5 days) or a combination of CyA and acyclovir. Blood levels of CyA were determined after a single dose. Urine was monitored for volume, osmolality, total protein and N-acetyl-beta-D-glucosaminidase (beta-NAG). Concentrations of blood urea nitrogen (BUN) and plasma-creatinine were determined (day 9). Renal cortical slices were monitored for accumulation of weak organic acids (para-aminohippurate, PAH) and bases (tetra-ethylammonium, TEA) and for malondialdehyde (MDA) content. Renal histology was also examined. CyA induced a decrease in body and kidney weight, in urine osmolality and in the excretion of total protein. Plasma-creatinine and BUN as well as MDA content of renal tissues were increased by CyA. Acyclovir alone did not induce significant changes. In comparison to CyA values, urine volume and beta-NAG excretion were enhanced and TEA accumulation depressed by the concomitant administration of CyA and acyclovir. CyA- or acyclovir-treatment alone did not result in significant morphological changes. In the group co-administered CyA/acyclovir, the kidneys showed mild to moderate signs of tubulopathy. Short-term co-administration of CyA and acyclovir was concluded to have possibly increased nephrotoxic potential.

Acetylglucosaminidase↗
PubMed1975

Functional characteristics of the renal tubular secretion of amprolium, a quaternary organic base.

Amprolium [1-(4-amino-2-propyl-5-pyrimidinemethyl)-2-methyl-pyridinium chloride hydrochloridel is a basic (quaternary) organic compound. At very low plasma concentration, it is cleared by the kidney at a rate approximating renal plasma flow in the dog. Its renal clearance is not depressed by organic acids (p-aminohippurate or probenecid) but is reduced by the quaternary base, mepiperphenidol. Acetate and pantothenate may influence the clearance of amprolium but, if this is the case, the effect is less than for p-aminohippurate. Its clearance is depressed as urinary pH is increased. The clearance of amprolium was not altered over a substantial range in urine flow at either high or low urinary pH.

Acetates↗
PubMedDate not supplied

Clinical, biochemical and histochemical studies on infants with Acrodermatitis enteropathica chronica.

7 infants diseased with Acrodermatitis enteropathica and 10 normal controls were included in this study. The values of anthranilic acid glucuronide, 6- aminohippuric, anthranilic acid, N-acetyl Kneurine, Kneurine and 30 H Kneurenine, were estimated in mg/24 hours urine, both basal and after tryptophane load. In addition, histopathological and histochemical studies for lactase, succinic dehydrogenase, alkaline phosphatase, acid phosphatase, and alpha-non-specific esterases activities were done for the intestinal mucosal biopsies. All the previous investigations were then repeated after two months treatment with 500 mg/day diiodohydroxyquinoline. The tryptophan metabolites were significantly low in the diseased infants, both basal and after tryptophan load. Moreover, the intestinal enzymes activities were altered. After 2 months treatment with diiodohydroxyquinoline the diseased infants became clinically improved, tryphtophan metabolites became normal, but the activities of the intestinal enzymes were not altered. The biochemical and histochemical findings were discussed, giving the possibility of competitive inhibition of the diiodohydroxyquinolines and the by-product 8 OH Quinololic acid resulting in more degradation of Kneurine and 3 OH Kneurenine to nicotinamide adenine dinucleotide.

Acrodermatitis↗