Urinary hypoxanthine and xanthine levels in acute coronary syndromes

Abstract

Ischemia leads to impaired ATP metabolism, with increased production of purine degradation products, such as hypoxanthine and xanthine, which are useful markers of tissue hypoxia. These extracellular markers of ischemia have been studied extensively in many clinical conditions of oxidative stress, including perinatal asphyxia, acute respiratory distress syndrome, cerebral ischemia, and preeclampsia. The aim of this study was to explore the usefulness of urinary hypoxanthine and xanthine as ischemia markers in acute coronary syndromes. Urinary excretion of hypoxanthine and xanthine was assessed by high-performance liquid chromatography in 30 patients with acute coronary syndromes and in 30 age- and sex-matched controls. Serum and urine uric acid, creatinine, and urea concentrations were also determined. Hypoxanthine excretion was significantly elevated in patients compared with healthy controls (84.37+/-8.63 and 42.70+/-3.97 nmol/mg creatinine, mean+/-SEM, P<0.0001). Urinary xanthine levels were also increased in patients with acute coronary syndromes (100.13+/-12.14 and 34.74+/-4.07 nmol/mg creatinine patients and controls, respectively; P<0.0001). Hypoxanthine and xanthine excretion showed a strong positive correlation in both groups. Significant negative correlations between urinary hypoxanthine and uric acid and xanthine and uric acid were observed in the patients, but not in controls. In conclusion, increased levels of ATP degradation products hypoxanthine and xanthine are observed in various hypoxic clinical conditions. This study suggests that these parameters may be useful markers of ischemia in patients with acute coronary syndromes.

Are CVD Patients Under Oxidative Stress?

“…A summary of the results is given in Fig. 2 (Akkus et al, 1996;Cavalca et al, 2001;Chiu et al, 1994;Cipollone et al, 2000;Clejan et al, 2002;Delanty et al, 1997;Durak et al, 2001;Ferns et al, 2000;Gackowski et al, 2001;Haidari et al, 2001;Halevy et al, 1997;Karmansky et al, 1996;Kesavulu et al, 2001;Kostner et al, 1997;McMurray et al, 1992;Schisterman et al, 2002;Singh et al, 1995;Tamer et al, 2002;Turgan et al, 1999;Weinbrenner et al, 2003). Fig.…”

Cell-free plasma DNA and purine nucleotide degradation markers following weightlifting exercise

“…During recirculation, following the termination of acute exercise and following these temporary bouts of ischemia, hypoxanthine serves as substrate for superoxide radical production by xanthine oxidase (McCord 1985;Rietjens et al 2007). Based on this Turgan et al 1999 suggest that xanthine oxidase (XO) and its substrates, hypoxanthine and xanthine, contribute to oxidative stress (Turgan et al 1999).…”

Metabolite profiling of blood from individuals undergoing planned myocardial infarction reveals early markers of myocardial injury

“…Finally, metabolite changes observed in humans modulated the response to hypoxic injury in vitro, which suggests that these metabolites not only serve as markers, but may also modulate the evolving response to ischemia in vivo. The metabolic, structural, and functional consequences of ischemia and/or reperfusion have been examined in a wide variety of experimental animal models, including regional ischemia after coronary vessel occlusion in dogs (29)(30)(31) and swine (32)(33)(34)(35) as well as in humans with coronary disease (36)(37)(38)(39)(40) or undergoing heart surgery (41-43). However, prior studies have generally assayed relatively limited subsets of metabolites in focused approaches.…”