PT  - JOURNAL ARTICLE
AU  - BERNARD STEINETZ
AU  - THOMAS GIANNINA
AU  - MARGARET BUTLER
TI  - THE ROLE OF SULFHYDRYL GROUPS IN THREE MODELS OF INFLAMMATORY DISEASE
DP  - 1973 Apr 01
TA  - Journal of Pharmacology and Experimental Therapeutics
PG  - 139--149
VI  - 185
IP  - 1
4099  - http://jpet.aspetjournals.org/content/185/1/139.short
4100  - http://jpet.aspetjournals.org/content/185/1/139.full
SO  - J Pharmacol Exp Ther1973 Apr 01; 185
AB  - The role of sulfhydryl (SH) groups in the etiology and therapy of acute and chronic inflammation has been studied in three different rat models: carrageenin-induced paw edema, the croton oil-induced granuloma pouch and the adjuvant-induced polyarthritis. Carrageenin edema was inhibited by indomethacin but not by locally or systemically injected thiols. However, subplantar injection of the SH-binding reagent, N-ethylmaleimide, produced a profound edema which was inhibited by cysteine but by indomethacin. Thus there are both thiol-dependent and independent types of edema. Injection of N-ethylmaleimide into granuloma pouches inhibited exudation. Cysteine reversed this effeet, which suggests that the protein synthesis necessary for exudative granuloma formation is thiol-dependent. Adjuvant injection in rats was followed by a depression of the serum sulfhydryl-disulfide (SH-SS) interchange reaction and the appearance of an abnormal serum α-2 glycoprotein, well before the onset of frank arthritis. Tissue (paw) SH levels showed no change. Anti-inflammatory compounds, but not SH donors, restored to normal the impaired serum SH-SS interchange reactions, inhibited the rise in abnormal protein level and suppressed arthritic symptoms. The depressed SH-SS interchange reaction thus appears to be a consequece of, rather than an etiological factor in adjuvant disease. Thus, thiols may be either pro- or anti-inflammatory or have no effect, depending entirely on the model selected for study. © 1973 by The Williams & Wilkins Company