Reference

Effect of antiinflammatory drugs on lysosomes and lysosomal enzymes from rat liver

Effect of antiinflammatory drugs on lysosomes and lysosomal enzymes from rat liver.Some chemicals with cas registry numbers like 2203-97-6 and 530-78-9 are also used. Smith, Robert J.; Sabin, Crawford; Gilchrest, Helen; Williams, Shirley (Dep. Physiol., Schering Corp., Bloomfield, N. J., USA). Biochem. Pharmacol., 25(19), 2171-7 (English) 1976. CODEN: BCPCA6. DOCUMENT TYPE: Journal CA Section: 1 (Pharmacodynamics) Section cross-reference(s): 7 The in vitro membrane stability of lysosomes from a heavy mitochondrial (3500 g) rat liver fraction was greatly increased by naproxen [22204-53-1], alclofenac [22131-79-9], chloroquine phosphate [50-63-5], mefenamic acid [61-68-7], phenylbutazone [50-33-9], hydrocortisone hemisuccinate [2203-97-6], dexamethasone dihydrogen phosphate [312-93-6], and methylprednisolone hemisuccinate [2921-57-5] (all at 10-6-10-3M). Ibuprofen [15687-27-1] and flufenamic acid [530-78-9] were moderately stabilizing and indomethacin [53-86-1], aspirin [50-78-2], and clonixin [17737-65-4] showed weak activity. Hydrocortisone, dexamethasone, paramethasone acetate [1597-82-6], and esp. chloroquine, inhibited aryl sulfatase [9016-17-5], and phenylbutazone, but no steroids, inhibited .beta.-glucuronidase [9001-45-0]. Antiinflammatory drugs may therefore inhibit the release of enzymes from lysosomes, and some may also inhibit lysosomal enzymes. .

Modulation of phagocytosis by and lysosomal enzyme secretion from guinea-pig neutrophils: effect of nonsteroid anti-inflammatory agents and prostaglandins

Modulation of phagocytosis by and lysosomal enzyme secretion from guinea-pig neutrophils: effect of nonsteroid anti-inflammatory agents and prostaglandins. Smith, Robert J. (Dep. Physiol., Schering Corp., Bloomfield, N. J., USA). J. Pharmacol. Exp. Ther., 200(3), 647-57 (English) 1977. CODEN: JPETAB. DOCUMENT TYPE: Journal CA Section: 1 (Pharmacodynamics) Guinea-pig neutrophils released lysosome granule-assocd. .beta.-glucuronidase [9001-45-0], but not cytoplasmic lactate dehydrogenase during cell contact with and phagocytosis of serum-treated zymosan particles.There are some reagents with their cas registry numbers 9001-45-0 and 22204-53-1 are used in this study. Naproxen [22204-53-1], chloroquine phosphate [50-63-5], and indomethacin [53-86-1] inhibited particle uptake by and lysosomal enzyme secretion from neutrophils incubated with zymosan in Krebs-Ringer phosphate medium, pH 7.4, at 37.degree.. Acetylsalicylic acid [50-78-2], fenoprofen [31879-05-7] and ibuprofen [15687-27-1] were inactive. The prostaglandins, PGE1 [745-65-3], PGE2 [363-24-6], PGA1 [14152-28-4], PGA2 [13345-50-1], PGB1 [13345-51-2], and PGB2 [13367-85-6], reduced particle ingestion by and discharge of lysosomal enzymes from neutrophils. PGF2.alpha. [551-11-1] accelerated lysosomal enzyme release, had no effect on phagocytosis at high concns., and inhibited both processes at low concns. PGF1.alpha. [745-62-0] was inactive. In the presence of cytochalasin B, an agent which inhibits phagocytosis while having no effect on selective lysosomal enzyme secretion, naproxen, chloroquine, and indomethacin, continued to inhibit the discharge of .beta.-glucuronidase from neutrophils. PGE1, PGE2, PGA1, PGA2, PGB1 and PGB2 reduced lysosomal enzyme release from cytochalasin B-treated neutrophils. PGF2.alpha. accelerated at high and inhibited at low concns. the selective secretion of .beta.-glucuronidase from cytochalasin B-treated neutrophils. PGF1.alpha. was again inactive. Thus, guinea-pig neutrophils are capable of a selective release of lysosomal enzymes (.beta.-glucuronidase) during ingestion of serum-treated zymosan particles and certain-inflammatory drugs and prostaglandins may function as modulators of the phagocytic release of lysosomal enzymes from neutropils. .