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Biomedical subjects

C C Funder

Publications and source records attributed to C C Funder.

16 recordsLinked to original sources
PubMed1978

Liver and kidney damage induced by N-hydroxyparacetamol.

1. Liver and kidney glutathione are depleted in rats and mice following administration of N-hydroxyparacetamol. 2. Centrilobular hepatic necrosis and necrosis of renal proximal convoluted tubules were also found, the liver lesion predominantly in mice and the renal lesion predominantly in rats. Glutathione depletion was not responsible for this species difference. 3. These results indicate that N-hydroxyparacetamol is the metabolic precursor of the reactive toxic intermediate of paracetamol. They are also relevant to the pathogenesis of the renal damage associated with long term abuse of phenacetin containing compound analgesics.

Acetaminophen↗
PubMed1977

An experimental model of analgesic-induced renal damage--some effects of p-aminophenol on rat kidney mitochondria.

1. p-Aminophenol, a known nephrotoxin, has been studied as a model for phenacetin-induced renal damage. 2. Respiration, oxidative phosphorylation and ATPase activity were inhibited in mitochondria isolated from the kidneys of treated rats; this could not be reversed by the addition of exogenous loosely bound cofactors and bovine serum albumin to the assay medium. 3. After treatment the mitochondrial levels of sodium and calcium were increased, potassium decreased and magnesium unaltered. 4. Mitochondria isolated from treated rats showed ultrastructural damage. 5. The results are interpreted to indicate that renal tubular cell mitochondrial injury is important in triggering cortical analgesic renal damage.

Adenosine Triphosphatases↗
PubMed1976

Neoplasia in the rat induced by N-hydroxyphenacetin, a metabolite of phenacetin.

N-hydroxyphenacetin, a phenacetin metabolite, was fed to rats as a 0.05-0.5% dietary supplement. After 9 months, tumours of the liver were found in 36 of 64 animals. One animal also developed a renal tumour. No tumours were found in control animals. The findings implicate phenacetin as a carcinogen and suggest that N-hydroxyphenacetin may be the metabolite responsible.

Animals↗
PubMed1975

Nephrotoxicity and molecular structure.

The nephrotoxicity of a number of aminophenols, quinols and catechols has been assessed from the extent of necrosis of proximal convoluted tubules produced by intravenous injection in rats, and the toxicity correlated with the oxidation-reduction potentials of the compounds.

Aniline Compounds↗
PubMed1971

Comparative nephrotoxicity of aspirin and phenacetin derivatives.

Both aspirin and phenacetin derivatives were shown to be nephrotoxic when administered to rats as a single intravenous injection. Phenacetin derivatives tended to produce more severe renal damage and to be nephrotoxic in smaller doses than aspirin derivatives. With the exception of a single derivative, the renal lesions were confined to the proximal convoluted tubule, even after administration of compounds which under other conditions have induced renal papillary necrosis.

Aniline Compounds↗