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Query: UMLS:C0265264 (HOS)
 1,119 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

During vertebrate evolution, structural changes in red blood cells (RBC) and hemoglobin (Hb), have probably resulted in the importance of blood carbon dioxide transport. The chloride/bicarbonate exchange across the RBC membrane, which is an integral part of the blood CO(2) transport process in vertebrates, has been examined on two different species of teleost fish, Euthynnus alletteratus and Thunnus thynnus, at several oxygenation states of erythrocyte HOS (high-oxygenation state, about 90 % of saturation) and LOS (low-oxygenation state, about 15 % of saturation). The results were compared with those observed in human RBC under the same experimental conditions and with the chicken (Gallus gallus) erythrocytes, which have particular modifications at the N-terminus of the band 3 protein (B3). In fish the kinetic measurements have shown a different anion transport in several oxygenation states of erythrocytes, indicating that also at lower levels of vertebrate evolution there exists a modulation of the anionic flow affected by oxygen. The functional correlation of anion transport to changes of parts of the hemoglobin sequence responsible for alterations in the interactions with the cytoplasmic domain of band 3 protein (cdb3) allowed us to suggest a hypothesis about fish physiology. The highest values of kinetic measurements observed in fish have been attributed to the metabolic need of the RBC in response to the removal of CO(2) that in teleosts is also of endogenous origin.
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PMID:Band 3 protein function in teleost fish erythrocytes: effect of oxygenation-deoxygenation. 1729 4

Carbon monoxide (CO), a by-product released during the degradation of heme by heme oxygenases (HOS EC 1.14.99.3) in animals, plays a major role as neurotransmitter, regulator of sinusoidal tone, inhibitor of platelet aggregation and suppressor of acute hypertensive response, and most of above effects are similar to or mediated by nitric oxide (NO), another signal molecule in both the animal and plant kingdoms. Previous result demonstrated that NO could act as a promoter of plant cell elongation, acting similarly to IAA, inducing morphogenetic responses leading to expansion in plant tissues. Recent observations revealed that CO is an inducer of cell expansion in wheat root segments, acting similarly to IAA and NO. Evidence also indicated that IAA could result in either the potent induction of HO-1 transcript or endogenous CO releasing in wheat root segments. Additionally, our results suggested that above CO signaling might be related to NO/cGMP, Ca(2+) and even ROS-dependent pathways. In this addendum, combined with other previous results, we further proposed a possible hypothesis for CO signaling role in regulation of plant root development induced by auxin.
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PMID:Carbon monoxide: A novel and pivotal signal molecule in plants? 1970 71

This study was designed to investigate the neuroprotective effect of hyperoxygenate hydrogen-rich saline (HOHS) against brain injury induced by carbon monoxide (CO) poisoning in rats. A rat model of CO poisoning was established by administering CO via intraperitoneal injection to male Sprague-Dawley rats. Forty-eight adult male rats were randomly divided into the following groups: normal control group (NG), CO poisoning group (CO), HOS treatment group (hyperoxygenated solution, HOS) and HOHS treatment group (HOHS). After CO poisoning, the carboxyhemoglobin (COHb) contents in the blood of rats in all the CO poisoning groups were increased significantly. However, HOS and HOHS significantly decreased COHb contents, furthermore, the HOHS group had lower COHb contents than the HOS group. Arterial oxygen partial pressure (PaO2) and arterial oxygen saturation (SaO2) results showed that HOS and HOHS could improve the oxygenation of the rats with CO poisoning. Compared with the CO group, the HOS group and the HOHS group had persistently neuroprotective effect on CO-induced brain injury, as assessed by modified neurological severity score (mNSS), furthermore, the HOHS group had better neurological functional recovery than the HOS group. The neuronal apoptosis induced by CO was also evaluated. Except the NG group, all the CO-poisoning groups had varying degrees of neuronal apoptosis. There was lesser degree of neuronal apoptosis in both the HOS group and the HOHS group than that in the CO group. Moreover, the HOHS group had more minor degree of neuronal apoptosis than the HOS group. Compared with the CO group, the free radicals production in the HOS group and the HOHS group were significantly inhibited. In addition, there were significantly difference in the free radicals production between the HOS group and the HOHS group. We could conclude that HOHS exerted a stronger neuroprotective effect against CO-induced brain injury than HOS, and the neuroprotective mechanism of HOHS may be related with inhibition of both neuronal apoptosis and free radicals.
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PMID:The neuroprotective effect of hyperoxygenate hydrogen-rich saline on CO-induced brain injury in rats. 3081 78