Inhibition of the formation of advanced glycation end products by thymoquinone

► Advanced glycation end products (AGEs) are associated with the development of chronic degenerative diseases including obesity, diabetes, Alzheimer’s, cardiovascular, and cancer. ► The efficacy of thymoquinone, against the formation of AGEs was investigated. ► Thymoquinone at concentration that is not toxic to normal cells inhibited the formation of early and late glycation of human serum albumin ex vivo. ► The potential of thymoquinone is the prevention of the development of human chronic diseases is discussed. The inhibitory activity of thymoquinone, a major quinone from black seeds (Nigella sativa) against the formation of advanced glycation end products was studied using the hemoglobin-δ-gluconolactone, human serum albumin–glucose, and the N-acetyl-glycyl-lysine methyl ester–ribose assays. A comparison was made with the inhibitory activity of aminoguanidine. The cytotoxicity of thymoquinone was studied by the release of lactate dehydrogenase from platelets and the levels of plasma thiols. At 20μM, thymoquinone inhibited 39% of hemoglobin glycation, 82% of post-Amadori glycation products, reduced methyglyoxal-mediated human serum albumin glycation by 68%, inhibited 78% of late glycation end products. Aminoguanidine at 10mM was less effective than thymoquinone. The IC50 for thymoquinone and aminoguanidine were 7.2μM and 1.25mM, respectively. Thymoquinone at 20–50μM was not toxic to platelet lactate dehydrogenase and plasma thiols. The potential of thymoquinone in food applications is discussed.