Carbonyl Traps as Potential Protective Agents against Methimazole‑Induced Liver Injury

Abstract

Liver injury is a deleterious adverse effect associated with methimazole administration, and reactive intermediates are suspected to be involved in this complication. Glyoxal is an expected reactive intermediate produced during methimazole metabolism. Current investigation was undertaken to evaluate the role of carnosine, metformin, and N-acetyl cysteine as putative glyoxal (carbonyl) traps, against methimazole-induced hepatotoxicity. Methimazole (100 mg/kg, intraperitoneally) was administered to intact and/or glutathione (GSH)-depleted mice and the role of glyoxal trapping agents was investigated. Methimazole caused liver injury as revealed by an increase in serum alanine aminotransferase and aspartate aminotransferase. Moreover, lipid peroxidation and protein carbonylation occurred significantly in methimazole-treated animals' liver. Hepatic GSH reservoirs were decreased, and inflammatory cells infiltration was observed in liver histopathology. Methimazole-induced hepatotoxicity was severe in GSH-depleted mice and accompanied with interstitial hemorrhage and necrosis of the liver. Glyoxal trapping agents effectively diminished methimazole-induced liver injury both in intact and/or GSH-depleted animals.

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“…Afterward, 2 mL of n-butanol was added and vigorously mixed. Finally, samples were centrifuged (3000 Âg for 5 min) and the absorbance of developed color in n-butanol phase was measured at 532 nm using an Ultrospec 2000 V R UV spectrophotometer (Uppsala, Sweden) [20].…”

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“…Afterward, 2 mL of supernatant was added to 4 mL of Tris buffer (pH= 8.9) and 100 µl of DTNB solution (0.01 M in methanol). 32,33 Finally, the samples absorbance was assessed at 412 nm using an Ultrospec 2000 ® UV spectrophotometer.…”

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“…Samples were centrifuged (3000 g for 5 minutes) and the absorbance of developed color in n-butanol phase was read at 532 nm using an Ultrospec 2000 ® UV spectrophotometer. 31…”