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© 1985 Oxford University Press

research-article

Degeneration of the Rat and Canine Adrenal Cortex Caused by {alpha}-(1,4-Dioxido-3-methylquinoxalin-2-yl)-N-methylnitrone (DMNM)

JOHN T. YARRINGTON, DAVID E. LOUDY, D. JEAN SPRINKLE, JOHN P. GIBSON, C. LEE WRIGHT and J. O'NEAL JOHNSTON

Merrell Dow Research Institute, Merrell Dow Pharmaceuticals Inc. Subsidiary of The Dow Chemical Company, Cincinnati, Ohio 45215

Degeneration of the Rat and Canine Adrenal Cortex Caused by {alpha}-(1,4-Dioxido-3-methylquin-oxalin-2-yl)-.Nmethylnitrone (DMNM). YARRINGTON, J. T., LOUDY, D. E., SPRINKLE, D. J., GIBSON, J. P., WRIGHT, C. L, and JOHNSTON, J. O. (1985). Fundam. Appl. Toxicol. 5, 370–381. The antibacterial druga {alpha}-(1,4-dioxido-3-methylquinoxalin-2-yl)-N-methylnitrone (DMNM) given at a dose of 22.5 mg/kg bid to four dogs for 14 days caused diminished adrenal cortical reserves as determined by decreased plasma cortisol (three dogs) and lower aldosterone levels (four dogs) following the intravenous infusion of ACTH. A dose of 100 mg/kg/day of DMNM administered to rats for 31 or 35 days resulted in significant decreases in blood glucose. Histologically, the adrenal glands of both species treated with DMNM for a maximum period of 21 days (dogs) and 35 days (rats) had widespread granular and vacuolar degeneration of the cortex. This degeneration in treated rats began in the zona reticularis and inner regions of the zona fasciculata and eventually involved the entire cortex including the zona glomerulosa. As a result of treatment, significant ultrastructural alterations within cells of the rat and canine adrenal cortex consisted of degeneration of the mitochondria and an increase in the numbers and lipolysis of lipid droplets. The ultrastructure of the zona reticularis and fasciculata was most severely affected.


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