Kirschbaum B
Department of Medicine, Medical College of Virginia, Virginia Commonwealth University, Richmond, VA 23298-0160, USA.
Med Hypotheses. 2001 Jun;56(6):625-9. doi: 10.1054/mehy.2000.1221.
Hyperuricemia has been labeled both a risk factor and marker for cardiovascular pathology in addition to being associated with gout and kidney disease. Uric acid in vitro acts as a potent antioxidant capable of scavenging hydroxy radicals and peroxynitrite and reacting with nitric oxide. Some clinical studies have provided evidence that, in vivo, uric acid is oxidized under conditions associated with high oxidant stress and may spare other antioxidants such as ascorbic acid. The plasma level of uric acid is controlled by the rates of production and excretion or degradation of uric acid. Under most circumstances, it is the renal clearance of uric acid which primarily determines the plasma concentration. Many factors of exogenous and endogenous origin can influence renal tubular absorption and secretion of uric acid. We suggest that renal urate clearance is not haphazard but regulated by an unknown signal that is issued in response to the level of oxidative stress. Since much cardiovascular pathology is now believed to have an inflammatory component and is associated with enhanced production of free radicals, the accompanying hyperuricemia may be viewed as a compensatory response of potential benefit.
高尿酸血症除了与痛风和肾脏疾病相关外,还被视为心血管疾病的危险因素和标志物。尿酸在体外是一种有效的抗氧化剂,能够清除羟基自由基和过氧亚硝酸盐,并与一氧化氮发生反应。一些临床研究表明,在体内,尿酸在高氧化应激条件下会被氧化,从而可能使其他抗氧化剂(如抗坏血酸)得以保留。尿酸的血浆水平受尿酸生成、排泄或降解速率的控制。在大多数情况下,主要是尿酸的肾脏清除率决定血浆浓度。许多外源性和内源性因素可影响肾小管对尿酸的重吸收和分泌。我们认为,肾脏尿酸清除并非随机发生,而是受一种未知信号调节,该信号根据氧化应激水平发出。由于现在认为许多心血管疾病都有炎症成分,且与自由基生成增加有关,因此伴随的高尿酸血症可被视为一种可能有益的代偿反应。