• Ning Li, Fei-yan Chen, and Qi-yi Zeng.
• Department of Neonatology, Nanfang Hospital, Southern Medical University, Guangzhou 510515, China. ningli@fimmu.com
• Nan Fang Yi Ke Da Xue Xue Bao. 2010 Jul 1;30(7):1569-72.

ObjectiveTo study the pathogenesis of adrenal mitochondrial dysfunction in septic rats.MethodsThirty SPF rats were randomized into 3 groups, including a normal control group and 2 sepsis groups receiving intraperitoneal injection of 10 mg/kg lipopolysaccharide (LPS) and observed at 6 and 24 h after the injection. The adrenal mitochondria were extracted from the rats at the corresponding time points for observation by electronic microscopy. The membrane potential of the mitochondria was detected by flow cytometry. The oxidative stress levels in the mitochondria (activities of NOS and levels of MDA and NO) were assessed.ResultsWith the progression of sepsis, the serum levels of corticosterone in LPS groups increased significantly as compared with that in the control group. Ultrastructural observation of the adrenal mitochondria showed mild mitochondrial injury in LPS groups in comparison with the control group. The mitochondrial membrane potential was lowered in the LPS groups, but all these changes appeared to be reversible. The activities of NOS and the levels of MDA and NO showed no significant difference between the sepsis groups and the control group.ConclusionsNo obvious adrenal dysfunction occurs in the early stage of sepsis in rats. Mitochondrial injury, which is reversible, occurs in early sepsis without obvious evidence of oxidative stress injury in the adrenal mitochondria, suggesting a strong resistance and capacity of self-repair of the adrenal gland and the mitochondria against sepsis-induced injury.

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