Skvortsova N N, Vysochina I V
Environ Health Perspect. 1976 Feb;13:101-6. doi: 10.1289/ehp.7613101.
Early energy changes in lungs, liver, and kidneys during the introduction of a benz a pyrene and phenol (as the possible carcinogen activator) were studied. It was observed that 10 days after a single instance introduction of 5 mg benz a pyrene per 0.9% NaCl (60 rats), oxidative phosphorylation in the lungs and livers is disturbed in the test rats, accompanied by a reduction of adenine nucleotides in these tissues. It is assumed that at this stage, the detoxication of benz a pyrene is intensified by free oxidation systems and by the respiratory chain of mitochondria. A chronic 3-month exposure to benz a pyrene and phenol (150 rats, each 5 mg of benz a pyrene per month intratracheally and 0.4 mg/m3 of phenol round-the-clock) results in greater disturbances of the energy exchange in the lungs, liver and kidneys. Benz a pyrene and phenol, individually and in combination, inhibit oxidative phosphorylation in the lungs. This significantly decreases the content of adenine nucleotides in this tissue. Activation of anaerobic glycolysis (twofold) and of aerobic glycolysis (eightfold) does not make up for the energy insufficiency in the tissue. The effect of benz a pyrene and phenol in the liver also results in suppressing oxidative phosphorylation and in the activation of glycolysis (anaerobic 2.5 times, the aerobic 3.7 times). Changes in the bioenergy of the kidneys are not as great. Phenol in its combined effect with benz[a]pyrene intensifies the effect of the latter, as shown primarily to the greater activation of anaerobic and aerobic glycolysis in the lungs and livers of test rats. The observed disturbances as concern the weight dynamics of the animals (weight loss in test rats), vitamin metabolism (their decrease in the organs in in urine) and hemopoiesis of red blood cells (erythropenia) attest to the toxic effect of benz a pyrene phenol on the organism, which is greater in the case of the combined action of the studied agents. No changes were discerned in the morphology of white blood cells.
研究了在引入苯并[a]芘和苯酚（作为可能的致癌物激活剂）过程中，肺、肝和肾早期的能量变化。观察到，在每只0.9%氯化钠溶液中单次引入5毫克苯并[a]芘（60只大鼠）10天后，试验大鼠的肺和肝脏中的氧化磷酸化受到干扰，同时这些组织中的腺嘌呤核苷酸减少。据推测，在此阶段，苯并[a]芘的解毒作用通过自由氧化系统和线粒体呼吸链得到加强。对150只大鼠进行为期3个月的苯并[a]芘和苯酚慢性暴露（每月经气管内给予每只5毫克苯并[a]芘，全天候给予0.4毫克/立方米苯酚），导致肺、肝和肾中能量交换的更大紊乱。苯并[a]芘和苯酚单独及联合使用均抑制肺中的氧化磷酸化。这显著降低了该组织中腺嘌呤核苷酸的含量。无氧糖酵解（两倍）和有氧糖酵解（八倍）的激活并不能弥补组织中的能量不足。苯并[a]芘和苯酚对肝脏的作用也导致氧化磷酸化受到抑制以及糖酵解被激活（无氧糖酵解2.5倍，有氧糖酵解3.7倍）。肾脏生物能量的变化没有那么大。苯酚与苯并[a]芘联合作用时会增强后者的作用，主要表现为试验大鼠肺和肝脏中无氧和有氧糖酵解的更大激活。观察到的与动物体重动态（试验大鼠体重减轻）、维生素代谢（器官中维生素减少以及尿中维生素减少）和红细胞造血（红细胞减少）相关的紊乱证明了苯并[a]芘和苯酚对机体的毒性作用，在研究的两种物质联合作用时毒性作用更大。未发现白细胞形态有变化。
