Xanthine oxidase (XO) and aldehyde oxidase (AO) are molybdenum-dependent flavoenzymes involved in purine catabolism and hepatic xenobiotic metabolism. This study aimed to assess XO and AO activities and molybdenum (Mo) content in liver tissue from liver graft donors and recipients with end-stage liver failure (ESLF). Liver tissue samples were obtained from 10 liver donors (LD; control group) and 30 patients with ESLF undergoing liver transplantation. The ESLF cohort was further divided by primary liver disease: hepatitis B or C viral infection (HBV/HCV), alcohol-associated liver disease (ALD), primary sclerosing cholangitis (PSC), Wilson’s disease (WD), and primary biliary cholangitis (PBC). Enzymatic activity was determined by spectrofluorometry, and hepatic Mo content was measured by inductively coupled plasma mass spectrometry. Compared with LD controls, ESLF recipients showed a significant decrease in both hepatic XO activity and Mo content. At the subgroup level, XO activity was significantly reduced in ALD, PSC, and PBC, whereas HBV/HCV and WD showed lower but non-significant values. Mo content was significantly reduced in the overall ESLF cohort and in the WD subgroup, although disease-specific variability was observed, including relatively high Mo content in PSC. AO activity was assessed in a subset of samples and did not differ significantly between donor and recipient liver tissues. Correlation analyses did not demonstrate a statistically significant association between hepatic Mo content and XO activity, suggesting that total tissue Mo content may not directly reflect Mo-dependent enzymatic activity. These findings indicate that ESLF is associated with altered hepatic trace-element composition, including Mo, and with disturbances in Mo-dependent enzymatic activity. Future studies should combine liver tissue analysis with matched serum and portal blood samples to better characterise hepatic Mo metabolism and the systemic biological effects of trace elements.
Adamus et al. (Sun,) studied this question.