Impact of rising temperature on physiological and biochemical alterations that affect the viability of blood cells in American bullfrog crossbreeds.

The study aimed to examine the impact of increasing environmental temperatures on physiological changes, oxidative stress, nitric oxide production, total antioxidant capacity, and blood cell viability in American bullfrog crossbreeds. Frogs and frog blood cells were exposed to temperature ranges of 25-33 °C and 25-37 °C, respectively. Physiological parameters (body temperature, pulse rate, ventilation rate, and oxygen saturation) and biochemical parameters (total antioxidant power, hydrogen peroxide, malondialdehyde, nitric oxide, and mitochondrial activity) were measured at every 2 °C increment. Results showed that body temperature rose with increased environmental temperature (P < 0.05). Pulse rates at 33 °C were higher than those at 25-31 °C (P < 0.05). Ventilation rates at 31 °C exceeded those at 25 °C and 27 °C (P < 0.05). Oxygen saturation levels remained stable at 25-33 °C (P > 0.05). Total antioxidant power at 25 °C was greater than at 27-37 °C (P < 0.05). Hydrogen peroxide levels at 27 °C were higher compared to 25 °C and 31-37 °C (P < 0.05). Malondialdehyde levels at 25-33 °C were higher than at 35 °C and 37 °C (P < 0.05). Nitric oxide levels at 37 °C were higher than at 25-33 °C (P < 0.05), and at 35 °C were higher than at 25-31 °C (P < 0.05). Blood cell viability at 25-31 °C was higher than at 37 °C (P < 0.05). These results suggest that at an environmental temperature of 33 °C, the frogs' body temperature approached 31 °C or higher, and were likely to be harmful to the frogs. Finally, the environmental temperature that caused frog blood cell death was 37 °C.

Estrogen modulates the skeletal muscle regeneration process and myotube morphogenesis: morphological analysis in mice with a low estrogen status.

The purpose of this study was to elucidate the functions of estrogen and two estrogen receptors (ERs; ERα and ERß) in the myoregeneration process and morphogenesis. Cardiotoxin (CTX) was injected into the tibialis anterior (TA) muscles of ovariectomized (OVX) mice to induce muscle injury, and subsequent myoregeneration was morphologically assessed. The diameter of regenerated myotubes in OVX mice was significantly smaller than that in intact mice at all time points of measurement. OVX mice also showed lower muscle recovery rates and slower speeds than did intact mice. ER protein levels showed a predominance of ERß over ERα in both intact and OVX states. The ERß level was increased significantly at 7 days after CTX injection in OVX mice and remained at a high level until 14 days. In addition, continuous administration of E2 to OVX mice in which muscle injury was induced resulted in a significantly larger diameter of regenerated myotubes than that in mice that did not receive estrogen. The results indicate that estrogen is an essential factor in the myoregeneration process since estrogen depletion delayed myoregeneration in injured muscles and administration of estrogen under the condition of a low estrogen status rescued delayed myoregeneration. The results strongly suggested that ERß may be a factor that promotes myoregeneration more than does ERα.

Absence of estrogen receptors delays myoregeneration and leads to intermuscular adipogenesis in a low estrogen status: Morphological comparisons in estrogen receptor alpha and beta knock out mice.

This study aimed to investigate the function of estrogen receptors (ERs) in myoregeneration and intermuscular adipogenesis. Ovariectomized (OVX) ERα knockout (KO) mice and ERß KO mice were used to assess the effect of estrogen on the myoregenerative process. Tibialis anterior muscle was collected on days 7, 10, and 14 after cardiotoxin injection to assess myotube morphology and adipogenesis area. Regenerated myotubes from OVX-ERß KO mice were consistently smaller in diameter than those from OVX-ERα KO and OVX-wild-type mice, whereas the adipogenesis area of OVX-ERß KO mice was consistently greater than that of the other types. Therefore, ERß may be an influential factor in promoting myoregeneration and adipogenesis inhibition compared to ERα.