Damage to biological tissues induced by radical initiator 2,2'-azobis(2-amidinopropane) dihydrochloride and its inhibition by chain-breaking antioxidants.
A water-soluble azo compound, 2,2'-azobis(2-amidinopropane) dihydrochloride, a well-known free radical initiator, was administered intraperitoneally to mice to study the toxicological effects on biological tissues in vivo and their inhibition by chain-breaking antioxidants. It caused damage to biological tissues without biotransformation. No specific target organ was observed. The most striking fine structural changes were the degeneration, swelling, and disruption of the endothelium lining cells of the capillaries in various organs. Furthermore, the death of lymphocytes in the lymphoid tissues and the fatty degeneration of the liver and kidneys have also been observed. Water-soluble chain-breaking antioxidants, such as 2-carboxy-2,5,7,8-tetramethyl-6-chromanol (a vitamin E analogue), uric acid, cysteine, and glutathione suppressed the above damage, whereas vitamin C was ineffective.
D000578:Amidines / Q000378:metabolism / Q000633:toxicity*; D000818:Animals; D000975:Antioxidants / Q000494:pharmacology*; D005609:Free Radicals; D007668:Kidney / Q000187:drug effects; D008099:Liver / Q000187:drug effects; D008221:Lymphoid Tissue / Q000187:drug effects; D008297:Male; D051379:Mice; D008813:Mice, Inbred ICR; D014527:Uric Acid / Q000494:pharmacology; D014810:Vitamin E / Q000494:pharmacology
D000578:Amidines; D000975:Antioxidants; D005609:Free Radicals; D014810:Vitamin E; D014527:Uric Acid; C046728:2,2'-azobis(2-amidinopropane)