It has been well established that advanced glycation end-products (AGEs) have a strong
correlation with diabetes and its secondary complications. Moreover, dicarbonyls, especially, methylglyoxal
(MG) and glyoxal, accelerate AGEs formation and hence, have potential roles in the pathogenesis
of diabetes. They can also induce oxidative stress and concomitantly decrease the efficiency of
antioxidant enzymes. Increased proinflammatory cytokines (tumor necrosis factor-α and interleukin-
1β) are secreted by monocytes due to the dicarbonyl-modified proteins. High levels of blood dicarbonyls
have been identified in diabetes and its associated complications (retinopathy, nephropathy and
neuropathy). This review aims to provide a better understanding by including in-depth information
about the formation of MG and glyoxal through multiple pathways with a focus on their biological
functions and detoxifications. The potential role of these dicarbonyls in secondary diabetic complications
is also discussed.
Keywords: Dicarbonyls, methylglyoxal, glyoxal, toxicity, detoxification, diabetic complications.
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