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In conclusion, various endogenous and exogenous pathophysiological mechanisms in patients with chronic kidney diseases lead to enhanced activity of oxidative enzymes such as xanthine oxidase (XO), myeloperoxidase (MPO), and the NADPH oxidase enzymes (NOX)

Bilirubin forms from haemoglobin breakdown in aged RBCs and converts heme to biliverdin, forming UCB which binds to albumin, uptakes by hepatocyte, and conjugates it via UGT1A1 , and these metabolites are either excreted in faeces or undergo oxidation to form urobilin and stercobilin, which contribute to the characteristic colours of urine and faeces

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To further explore this effect, we examined additional GGT inhibitors (acivicin and OU749) 45 but found that GGsTop was the most potent at blocking GGT activity (Fig