Recent evidences demonstrated that ingestion of several monoterpenes cause hepatic and renal damage due to impairment on mitochondrial energy production, eliciting a collapse on adenosine triphosphate (ATP) synthesis and consequently impairment on bioenergetic homeostasis. Thus, the aim of this study was to evaluate whether phosphotransfer network, catalyzed by creatine kinase (CK), adenylate kinase (AK), and pyruvate kinase (PK), can be a pathway to explain hepatic and renal bioenergetics homeostasis impairment due to thymol ingestion. Daily intake of thymol (40 mg/kg) significantly cause a decreased kidney weight and relative kidney weight compared to control group. The same dose of thymol inhibited renal cytosolic and mitochondrial CK activity as well as renal PK activity compared to control group. Finally, thymol (40 mg/kg) elicited a significant increase on renal reactive oxygen species and lipid damage levels, as well as an inhibition on antioxidant capacity against peroxyl radicals and non-protein thiol levels, which did not occur liver. Doses of 10 and 20 mg/kg of thymol administered orally for 30 consecutive days non-changed these variables. Based on these evidence, the data supported that intake of a high dose of thymol severely inhibits cytosolic and mitochondrial CK activity, a crucial enzyme to maintain cellular energy homeostasis. Moreover, high dietary thymol intake impaired communication between CK isoenzymes, which inhibits the attempts to regenerate ATP or to facilitate the CK/PCr shuttle to improve the intracellular ATP utilization and consumption. Moreover, the inhibition of renal CK and PK activities appears to be mediated by the renal oxidation of lipids and thiol groups, as well as by the reduction of the renal antioxidant capacity.

最近的证据表明，摄入数个单萜会由于线粒体能量产生受损而引起肝和肾损害，从而导致三磷酸腺苷（ATP）合成崩溃，进而导致生物能体内平衡受损。因此，本研究的目的是评估由肌酸激酶（CK），腺苷酸激酶（AK）和丙酮酸激酶（PK）催化的磷酸转移网络是否可以作为解释由于百里酚引起的肝和肾生物能稳态平衡的途径。摄取。与对照组相比，每天摄入百里酚（40 mg / kg）会明显降低肾脏重量和相对肾脏重量。与对照组相比，相同剂量的百里酚可抑制肾脏的胞质和线粒体CK活性以及肾脏PK活性。最后，百里酚（40 mg / kg）引起肾脏活性氧种类和脂质损伤水平的显着增加，以及对过氧化物自由基和非蛋白质硫醇水平的抗氧化能力的抑制，而肝脏中未发生过氧化。连续30天口服10和20 mg / kg百里酚的剂量不会改变这些变量。基于这些证据，数据支持高剂量百里酚的摄入会严重抑制胞质和线粒体CK的活性，这是维持细胞能量稳态的关键酶。此外，高膳食百里酚摄入量削弱了CK同工酶之间的交流，这抑制了ATP再生或促进CK / PCr穿梭以提高细胞内ATP利用率和消耗的尝试。而且，