科学家已经发现了泰诺或扑热息疼等非处方药中使用的止疼药对乙酰氨基酚可能有助于保护患者的肾脏不受氧化损伤以及严重肌肉损伤后经常发生的肾衰竭。这项研究可能帮助受到“撞击”损伤（例如车祸或者地震造成的损伤）导致肌肉损伤的患者的临床治疗。
Olivier Boutaud及其同事证明了对乙酰氨基酚能够防止血红素蛋白（例如肌红蛋白）产生的自由基的形成，这些血红素蛋白在肌肉组织损伤之后释放到了血液中。这组科学家发现，肌红蛋白在肾脏积累，在那里这些化合物产生了能够破坏细胞并引发肾衰竭的自由基。这组作者证明了对乙酰氨基酚能够通过减少自由基引起的脂质过氧化（它会导致细胞损伤）从而保护受伤的大鼠不产生肾衰竭。对乙酰氨基酚的这种效应是在这种药物的人类临床治疗浓度之内实现的。这项关于对乙酰氨基酚效应的研究可能应用于其它含有血红素的蛋白从细胞中释放出来的情况，包括心脏病发作、疟疾和镰状细胞病。
推荐原始出处：
PNAS February 1, 2010, doi: 10.1073/pnas.0910174107
Acetaminophen inhibits hemoprotein-catalyzed lipid peroxidation and attenuates rhabdomyolysis-induced renal failure
Olivier Boutauda,1,2, Kevin P. Mooreb,1, Brandon J. Reederc, David Harryb, Alexander J. Howieb, Shuhe Wanga, Clare K. Carneyd, Tina S. Mastersona, Taneem Amina, David W. Wrightd, Michael T. Wilsonc, John A. Oatesa,e, and L. Jackson Roberts IIa,e
Departments of aPharmacology,
eMedicine, and
dChemistry, Vanderbilt University, Nashville, TN 37232;
cDepartment of Biological Sciences, University of Essex, Colchester, Essex CO4 3SQ, United Kingdom; and
bDepartments of Medicine and Pathology, University College London Medical School, London NW3 2QG, United Kingdom
Hemoproteins, hemoglobin and myoglobin, once released from cells can cause severe oxidative damage as a consequence of heme redox cycling between ferric and ferryl states that generates radical species that induce lipid peroxidation. We demonstrate in vitro that acetaminophen inhibits hemoprotein-induced lipid peroxidation by reducing ferryl heme to its ferric state and quenching globin radicals. Severe muscle injury (rhabdomyolysis) is accompanied by the release of myoglobin that becomes deposited in the kidney, causing renal injury. We previously showed in a rat model of rhabdomyolysis that redox cycling between ferric and ferryl myoglobin yields radical species that cause severe oxidative damage to the kidney. In this model, acetaminophen at therapeutic plasma concentrations significantly decreased oxidant injury in the kidney, improved renal function, and reduced renal damage. These findings also provide a hypothesis for potential therapeutic applications for acetaminophen in diseases involving hemoprotein-mediated oxidative injury.
