N-acetyl-beta-D-glucosaminidase (NAG) and alanine aminopeptidase (AAP) excretion after acute administration of acetaminophen, salsalate and aspirin in rats.

The present study was performed to compare renal injury induced by high acute doses of both the nonacetylated salicylate, salsalate (SSA) and the acetylated salicylate, aspirin (ASA). As a marker of renal injury, urinary excretion of N-acetyl-beta-D-glucosaminidase (NAG) and alanine aminopeptidase (AAP) were measured after oral administration of 600 mg/kg of each drug. Other tests to detect renal injury were also performed. Serum salicylic levels after SSA or ASA were determined in a different experiment. Acetaminophen (APAP) was used as a standard of renal toxicity. Both drugs increase NAG and to a greater extent, AAP excretion. Proteinuria and polyuria appear after both drugs. Changes in urinary sodium and potassium were also shown. Our results support the view that both acetylated and non-acetylated salicylates induce renal injury at toxicological doses.

Urinary N-acetyl-beta-D-glucosaminidase as a marker of renal injury in adjuvant arthritis.

In the present study we have determined if renal damage occurs with adjuvant arthritis (AA). As a sensitive indicator of renal injury in tubular cells, urinary N-acetyl-beta-D-glucosaminidase (NAG) was measured at predetermined times after arthritis induction. Urinary protein, sodium and potassium excretion were also evaluated. NAG levels in arthritic animals were higher than those in healthy ones from day 12 after induction and the levels remained high during the study period. A significant positive correlation was noted between urinary NAG excretion and disease severity reflected by hind paw edema. Protein excretion also increased in arthritic animals but there was no correlation between urinary protein, NAG levels, and degree of inflammation. Changes in urine sodium and potassium levels did not reach statistical significance. Thus, we can conclude that some renal damage occurred in this experimental model of chronic inflammation.

Chronic inflammation induced by type I collagen in rats.

In this study we attempt to investigate if collagen type 1 from bovine Achilles tendon is capable of causing an inflammatory response. Thus, we immunized rats with a collagen emulsion injected in the right hind paw, via subplantar, and intradermally on the back. Seven days later, the rats were reimmunized by intradermal injection on the base of the tail with an identical emulsion. The inflammatory response was assessed by measuring the hind paw swelling of the rats every seven days for two months. We also analysed the levels of anticollagen antibodies in each rat during the experimental period. An indirect microELISA method was developed to determine collagen-specific-antibodies in rat serum. We observed a chronic inflammation in 41% of immunized rats. This pathology results in local swelling in the hind paw that remained for at least two months. This model was accompanied with the production of antibodies against collagen that appeared on day 14 after induction and remained during the study period (56 days). A positive correlation between swelling and antibody titre was observed.