Klangpetch Wannaporn, Noma Seiji, Igura Noriyuki, Shimoda Mitsuya
Graduate School of Bioresource and Bioenvironmental Sciences, Kyushu University, Fukuoka, Japan.
Biosci Biotechnol Biochem. 2011;75(10):1945-50. doi: 10.1271/bbb.110325. Epub 2011 Oct 7.
The heat inactivating effect of low-pressure carbonation (LPC) at 1 MPa against Escherichia coli was enhanced to 3.5log orders. This study aimed to investigate the mechanisms of this increase in heat inactivation efficiency. The increased inactivation ratio was found to be the result of LPC-induced heat sensitization. This sensitization was not due to any physical damage to the cells as a result of the treatment. Following the depletion of intracellular ATP, the failure of the cells to discard protons caused an abnormal decrease in the intracellular pH. However, in the presence of glucose, the inactivation ratio decreased. In addition, a further increase in inactivation of more than 2log orders occurred in the presence of the protein synthesis inhibitor chloramphenicol. Hence, the decreased heat resistance of E. coli under LPC was most likely due to a depletion of intracellular ATP and a decreased capacity for protein synthesis.
1兆帕压力下的低压碳酸化（LPC）对大肠杆菌的热灭活效果提高到了3.5个对数级。本研究旨在探究热灭活效率提高的机制。发现灭活率的提高是LPC诱导热敏化的结果。这种敏化并非由于处理对细胞造成任何物理损伤。细胞内ATP耗尽后，细胞无法排出质子导致细胞内pH异常降低。然而，在有葡萄糖存在的情况下，灭活率降低。此外，在蛋白质合成抑制剂氯霉素存在的情况下，灭活率进一步提高了2个多对数级。因此，LPC作用下大肠杆菌耐热性降低很可能是由于细胞内ATP耗尽以及蛋白质合成能力下降。
