Daily Eastern News: October 31, 2003

https://thekeep.eiu.edu/den_2003_oct/1015/thumbnail.jp

Влияние фракции до 5 кДа из мозга холодоадаптированных рыб на жизнеспособность карася серебряного в условиях холодового стресса

Дослiджено вплив фракцiї до 5 кДа з мозку холодоадаптованого карася срiбного Carassius auratus на життєздатнiсть та енергетичнi параметри у риб при холодовому стресi влiтку. Показано, що експозицiя при 5–6 ºС влiтку призводить до загибелi риб на 3-тю 5-ту добу i до iстотного зниження активностi ЛДГ, а також до пiдвищення вмiсту лактату та пiрувату. Встановлено, що фракцiя до 5 кДа забезпечує виживанiсть риб пiд час холодової аклiмацiї влiтку протягом 9 дiб, сприяє зниженню рiвня АТФ, а також нормалiзацiї активностi ЛДГ i кiлькостi лактату та пiрувату.The data on the influence of the fraction less than 5 kD from brain of the cold-adapted goldfish Carassius auratus upon viability and energetic indices in the fish during cold stress in summer are presented. Exposure at 5–6 ºС in summer resulted in death of the fish on the 3rd-5th day and in a significant drop in the LDH activity, as well as in an increase in lactate and pyruvate contents. It has been shown that the fraction less than 5 kD provided the survival of the fish during the cold acclimation in summer up to 9 days and promoted a reduction in the ATP level, as well as changes in the LDH activity and lactate and pyruvate quantities towards the normalization of these parameters

Daily Eastern News: October 31, 2003

https://thekeep.eiu.edu/den_2003_oct/1015/thumbnail.jp

Energy Metabolism in Uncoupling Protein 3 Gene Knockout Mice

Uncoupling protein 3 (UCP3) is a member of the mitochondrial anion carrier superfamily. Based upon its high homology with UCP1 and its restricted tissue distribution to skeletal muscle and brown adipose tissue, UCP3 has been suggested to play important roles in regulating energy expenditure, body weight, and thermoregulation. Other postulated roles for UCP3 include regulation of fatty acid metabolism, adaptive responses to acute exercise and starvation, and prevention of reactive oxygen species (ROS) formation. To address these questions, we have generated mice lacking UCP3 (UCP3 knockout (KO) mice). Here, we provide evidence that skeletal muscle mitochondria lacking UCP3 are more coupled (i.e. increased state 3/state 4 ratio), indicating that UCP3 has uncoupling activity. In addition, production of ROS is increased in mitochondria lacking UCP3. This study demonstrates that UCP3 has uncoupling activity and that its absence may lead to increased production of ROS. Despite these effects on mitochondrial function, UCP3 does not seem to be required for body weight regulation, exercise tolerance, fatty acid oxidation, or cold-induced thermogenesis. The absence of such phenotypes in UCP3 KO mice could not be attributed to up-regulation of other UCP mRNAs. However, alternative compensatory mechanisms cannot be excluded. The consequence of increased mitochondrial coupling in UCP3 KO mice on metabolism and the possible role of yet unidentified compensatory mechanisms, remains to be determined