Effect of indomethacin and naproxen on the metabolism of glycosaminoglycans.
Indomethacin and naproxen were examined regarding their effects on glycosaminoglycan metabolism in normal albino rats. The biosynthesis of sulphated glycosaminoglycans as evaluated by the uptake of [35S-]sulphate and the content of glycosaminoglycans were measured in specimens of skin, liver and kidney. The results indicated that the biosynthesis of sulphated glycosaminoglycans was significantly inhibited by both these drugs, thus reflecting their anti-inflammatory properties. The catabolism of glycosaminoglycans was followed by estimating the activities of lysosomal glycohydrolases, viz., beta-glucuronidase, beta-N-acetyl glucosaminidase and cathepsin D in liver, kidney and spleen and urinary excretion of hexosamine and uronic acid. The results, considered collectively, indicated that both indomethacin and naproxen depressed the metabolism of glycosaminoglycans.
D000118:Acetylglucosaminidase / Q000097:blood; D000818:Animals; D002402:Cathepsin D; D002403:Cathepsins / Q000097:blood; D005966:Glucuronidase / Q000097:blood; D006025:Glycosaminoglycans / Q000378:metabolism*; D007213:Indomethacin / Q000494:pharmacology*; D007668:Kidney / Q000201:enzymology; D008099:Liver / Q000201:enzymology; D008297:Male; D009288:Naproxen / Q000494:pharmacology*; D051381:Rats; D011922:Rats, Mutant Strains; D013154:Spleen / Q000201:enzymology; D013462:Sulfur Radioisotopes
D006025:Glycosaminoglycans; D013462:Sulfur Radioisotopes; D009288:Naproxen; D005966:Glucuronidase; D000118:Acetylglucosaminidase; D002403:Cathepsins; D002402:Cathepsin D; D007213:Indomethacin