Gasotransmitters: Novel Roles of Ancient Gases in the Plant Response to Temperature Stress / 中国生物化学与分子生物学报

Gas molecules including hydrogen sulfide, nitric oxide, carbon monoxide, ethylene, hydrogen gas, ammonia, methane, hydrogen cyanide, and sulfur dioxide were the main components of primitive atmosphere on the earth four billion years ago. Nowadays, these gases are viewed as gasotransmitters (GTs) in organisms, namely endogenously gaseous molecules. GTs not only regulate many physiological and pathological processes, such as breathing, blood pressure, learning, memory, and the inflammatory response in animals, but also play a key role in the stomatal movement, seed germination, plant growth, development, and response to environmental stress. In this review, we cover the current progress on the metabolism of GTs, their response to temperature stress in plants, and their general characteristics, anabolism, catabolism. In addition, we highlight the key role of the antioxidant system, the osmoregulation system, the ion balance system, the water balance system, heat shock proteins, post-translational modifications, and re-establishment and repair of biomembranes in the mitigation of oxidative stress, osmotic stress, ion stress, water stress, protein denaturation, and biomembrane injury induced by temperature stress. The alleviation of these injuries could increase the resistance of plants to high temperature and low temperature stresses. Furthermore, we summarize the interactions among GTs by initiating chemical reaction, regulating metabolic enzymes, competing target molecules, and triggering new signaling to modulate temperature stress tolerance in plants. The aim of this review is to drive the rapid progress on GTs in the field of plant biology in the future.

Heme oxygenase-1/carbon monoxide signaling participates in the accumulation of triterpenoids of / 浙江大学学报（英文版）（B辑：生物医学和生物技术）

Ganoderic triterpenoids (GTs) are the primary bioactive constituents of the Basidiomycotina fungus,

The Effect of Carbon Monoxide on L-type Calcium Channel Currents in Human Intestinal Smooth Muscle Cells

Carbon monoxide (CO) is low molecular weight oxide gas that is endogenously produced under physiological conditions and interacts with another gas, nitric oxide (NO), to act as a gastrointestinal messenger. The aim of this study was to determine the effects of exogenous CO on L-type calcium channel currents of human jejunal circular smooth muscle cells. Cells were voltage clamped with 10 mM barium (Ba2+) as the charge carrier, and CO was directly applied into the bath to avoid perfusion induced effects on the recorded currents. 0.2% CO was increased barium current (I (Ba) ) by 15+/-2% (mean+/-S.E., p 0.05). CO mediates inhibitory neurotransmission through the nitric oxide pathway. Therefore, to determine if the effects of CO on L-calcium channels were also mediated through NO, cells were incubated with N (G) -nitro-L-arginine (L-NNA, 1 mM), a nitric oxide synthase inhibitor. After L-NNA pretreatment, 0.2 % CO did not increase barium current (4+/-2% increase, n=6, p> 0.05). NO donor, SNAP (20 microM) increased barium current by 13+/-2% (n=6, p< 0.05) in human jejunal smooth muscle cells. These data suggest that CO activates L-type calcium channels through NO/cGMP dependant mechanism.

Carbon monoxide poisoning as an epigenetic factor for Leber's hereditary optic neuropathy

A 45-year-old Korean woman visited our hospital complaining of poor vision after carbon monoxide (CO) poisoning. We have confirmed the presence of a point mutation at position 11778 in the ND4 gene of mitochondrial DNA. This case suggests that CO poisoning may precipitate the clinical expression of Leber's hereditary optic neuropathy (LHON). To our knowledge, this would be the first case report of clinical expression of LHON precipitated by CO poisoning.

Effect of Hyperbaric Oxygen Therapy on the Neurotransmitter Changes in Carbon Monoxide Exposed Rat Striatum

The selective vulnerability of the basal ganglia to carbon monoxide(CO) is well recognized. And hyperbaric oxygen therapy(HBO) has long been accepted as a primary treatment for CO poisoning; however, the mechanism of action and objective methods to assess the therapeutic efhcacy of HBO have not been fully established. To evaluate the effect of HBO on the neurotransmitter changes in CO poisoning the striatal dopamine and its metabolites were measured in CO-intoxicated and HBO treated rats by high performance liquid chromatograpy with electrochemical detection. Male SpragueDawley rats, weighing 250-350 g were exposed to 4,500 ppm CO for 30 minutes and a group of them was treated with HBO(3 ATA, 30 miutes). The neostriatum of the rats were obtained and investigated according to the various time lapse after the cessation of CO exposure or the completion of HBO, The results are as follows: 1. The application of the routine HBO to the normal rat did not affect the levels of striatal neurotransmitters. 2. The concentration of striatal DA was markedly increased in CO-intoxicated rat during acute phase and it was reversed by HBO. But the effect did not last more than 24 hours. 3. In the delayed phase of experiment, the concentration of striatal DA tended to be decreased, which was partially thought to be due to the striatal injury, damage of striatonigral pathway or neuronal loss of substantia nigra by C0-intoxication.These results suggest that dopaminergic system might be implicated both in the pathogenesis of C0-induced striatal injury and the therapeutic efficacy of HB0.

Cytogenetic Effects on Mouse Fetus of Acute and Chronic Transplacental In Vivo Exposure to Carbon Monoxide: Induction of Micronuclei and Sister Chromatid Exchanges

Carbon monoxide gas is found in the atmosphere whenever society has become industrialized. In addition to the fact that Korea has become industrialized, bituminous coal is used to heat homes here, in heating systems that, if not very carefully maintained, leak this gas, resulting in a number of deaths and near deaths each winter. It has only rarely been reported by investigators that genetic damage may be done transplacentally to a human fetus by a pregnant woman's being poisoned by CO. We explored this by evaluating the damage done to the mouse fetus through an in vivo experiment, using micronucleus and sister chromatid exchange (SCE) tests. Mice were mated and pregnant ones divided into a group that received acute exposures on 3 different days, a group that received chronic exposure, and a control group. In the meantime in the control group the incidence of both micronuclei and SCE was less on the maternal side, in both the acute and chronic exposure groups, whereas the incidences of both micronuclei and SCE were more on the maternal side. However, the incidence on the fetal side was not far behind. Increasing, the dosage of carbon monoxide with gestational age increased the incidence of both micronuclei and SCE in the mother and fetus alike.