Borrelia Species Detected in Ticks Feeding on Wild Korean Water Deer (Hydropotes inermis) Using Molecular and Genotypic Analyses.

Lyme borreliosis is a vector-borne disease transmitted through the bite of ticks infected by Borrelia burgdorferi sensu lato group, including B. burgdorferi sensu stricto, B. afzelii, and B. garinii. The goal of the present study was to detect Borrelia species in ticks infesting wild Korean water deer (KWD; Hydropotes inermis Swinhoe), using molecular and genotypic analyses. In total, 48 ticks were collected from KWD, all of which were morphologically identified as Haemaphysalis longicornis Neumann that is dominant in Korea. Nested PCR was performed to detect the Borrelia-specific 5S (rrf)-23S (rrl) intergenic spacer region and the outer surface protein A (ospA) genes in ticks. Both rrf-rrl and ospA were amplified from one of the 48 ticks (2.1%) and were identified as B. afzelii. To our knowledge, this study constitutes the first molecular detection of B. afzelii in Haemaphysalis ticks in Korea. Because B. afzelii is a zoonotic tick-borne pathogen, understanding the molecular characteristics of this bacterium is important for preventing the transmission of Borrelia from ticks to other animals and humans.

S-adenosylmethionine protects post-ischemic mitochondrial injury in rat liver.

BACKGROUND/AIMS: S-adenosylmethionine (SAM) is a thiol-containing compound with known therapeutic affects on cholestasis and hepatotoxicity. The aim of this study was to investigate the effect of SAM on the prevention of mitochondrial injury induced by hepatic ischemia and reperfusion. METHODS/RESULTS: Rats were subjected to 60 min of hepatic ischemia and 1 and 5 h of reperfusion. 2 h prior to ischemia, the animals received either vehicle or SAM intraperitoneally. In the vehicle-treated ischemic animals, serum aspartate aminotransferase levels increased at 1 h and again at 5 h of reperfusion and were reduced by SAM pre-treatment. Similarly, mitochondrial lipid peroxidation was elevated in the vehicle-treated group, but this elevation was attenuated by SAM. In contrast, mitochondrial glutamate dehydrogenase activity and reduced glutathione concentration both decreased in the vehicle-treated group, and this decrease was also inhibited by SAM. Hepatic ATP levels in the vehicle-treated rats were found to be 42% lower 5 h after reperfusion, however, treatment with SAM elevated these ATP levels. SAM treatment increased the concentration of adenosine but inhibited the accumulation of hypoxanthine in the ischemic liver. CONCLUSION: SAM protects against mitochondrial injury, which prevents mitochondrial oxidant stress and improves ischemia-induced hepatic energy metabolism.

Protective effect of allopurinol on hepatic energy metabolism in ischemic and reperfused rat liver.

Reactive oxygen species generated by xanthine oxidase during reperfusion of ischemic liver might in part be responsible for ischemic organ injury. In normothermic ischemia/reperfusion rat model, we investigated whether allopurinol pretreatment improved ischemia-induced mitochondrial dysfunction. Rats were subjected to 60 min of hepatic ischemia and to 1 h and 5 h of reperfusion thereafter. At 18 h and 1 h before ischemia, the animals received 0.25 mL of either saline or allopurinol (50 mg/kg) i.p. In saline-treated ischemic rats, serum aspartate aminotransferase levels increased significantly at 5 h (4685 +/- 310 IU/L) and were significantly reduced with allopurinol pretreatment. Similarly, mitochondrial lipid peroxidation was elevated in the saline-treated ischemic group, but this elevation was prevented by allopurinol. In contrast, mitochondrial glutamate dehydrogenase activity and ketone body ratio decreased in the saline-treated group, but this decrease was also inhibited by allopurinol. Hepatic ATP levels in the saline-treated rats were 42% lower 5 h after reperfusion. However, treatment with allopurinol resulted in significantly higher ATP levels. Allopurinol treatment preserved the concentration of AMP in ischemic liver but inhibited the accumulation of xanthine in reperfused liver. Our findings suggest allopurinol protects against mitochondrial injury, which prevents a mitochondrial oxidant stress and lipid peroxidation and preserves the hepatic energy metabolism.