Anti-HYOU1 (aa 901-999) polyclonal antibody

Background: Antarctic marine organisms have evolved a variety of physiological, life-history and molecular adaptations that allow them to cope with the extreme conditions in one of the coldest and most temperature-stable marine environments on Earth. The increase in temperature of the Southern Ocean, product of climate change, represents a great challenge for the survival of these organisms. It has been documented that some Antarctic marine invertebrates are not capable of generating a thermal stress response by means of an increase in the synthesis of heat shock proteins, which could be related with their low capacity for acclimatization. In order to understand the role of heat shock proteins as a compensatory response in Antarctic marine species to projected scenarios of increased seawater temperatures, we assessed the expression of the genes Hsp90, Grp78, Hyou1 and Hsc70 in the Antarctic sea urchin Sterechinus neumayeri under three thermal treatments (1 degrees C, 3 degrees C and 5 degrees C), for a period of exposure of 1, 24 and 48 h. Results: The results obtained showed that these genes were expressed themselves in all of the tissues analyzed in a constitutive form. During acute thermal stress, an overexpression of the Hsp90, Grp78 and Hyou1 genes was observed in coelomocyte samples at 3 degrees C after 48 h, while in esophageal samples, an increase in Hsp90 and Grp78 expression was observed after 48 h. Thermal stress at 5 degrees C, in general, did not produce a significant increase in the expression of the genes that were studied. The expression of Hsp70 did not show modifications in its expression as a result of thermal stress. Conclusions: S. neumayeri is capable of overexpressing stress proteins as a result of thermal stress, however, this response is delayed and to a lesser degree compared to other Antarctic or temperate species. These results indicate that adult individuals could cope with the expected impacts caused by an increase in coastal sea temperatures in the Southern Ocean.

To clarify whether sexual arousal could be enhanced by hypoxia, and to explain the pathogenesis of autoerotic death (AED)/autoerotic asphyxiation (AEA), we investigated the molecular-biological and hormonal interactions in male rats between hypoxia (10% O-2) and sexual stimulation (placing male rats with oestrous female rats) using hypothalamus tissue and serum. Serum oxytocin concentration was significantly increased by either hypoxia or sexual stimulation without significant change of Oxt mRNA expression. Serum concentration of adrenocorticotropic hormone was significantly elevated by sexual stimulation, although serum concentration of copeptin was significantly suppressed by hypoxia. Moreover, serum concentration of luteinising hormone was increased by hypoxia. These results suggested that hypoxia would complicatethe response to sexual stimulation, and effect a change in sexual arousal. Moreover, sexual stimulation significantly suppressed mRNA expressions of Hspa4 and Hyou1, which might indicate that sexual stimulation reducestolerance to hypoxia/ischaemia. Accordingly, it is possible that AED/AEA would be attributed to a reduced tolerance to hypoxia/ischaemia induced byattempts to obtain sexual arousal under a hypoxic condition and would not be a simple accident.