Sulfur dioxide appears as a colorless gas with a choking or suffocating odor. Boiling point -10°C. Heavier than air. Very toxic by inhalation and may irritate the eyes and mucous membranes. Under prolonged exposure to fire or heat the containers may rupture violently and rocket. Used to manufacture chemicals, in paper pulping, in metal and food processing. Rate of onset: Immediate & Delayed Persistence: Minutes to hours Odor threshold: 1 ppm Source/use/other hazard: Disinfectant and preserving in breweries and food/canning; textile industry; batteries.
颜色/状态：
Colorless gas or liquid
气味：
Strong suffocating odor
味道：
Acid taste
蒸汽密度：
2.264 at 0 °C (Air = 1)
蒸汽压力：
Vapor pressure (kPa): 230 at 10 °C; 330 at 20 °C; 462 at 30 °C; 630 at 40 °C
亨利常数：
Henry's Law constant = 8.10X10-4 atm-cu m/mol at 25 °C
稳定性/保质期：
Extremely stable to heat, even up to 2000 °C
自燃温度：
Not flammable (USCG, 1999)
粘度：
Gas: 0.0124 mPa.s at 18 °C. Liquid: 0.368 mPa.s at 0 °C.
腐蚀性：
Iron, steel, nickel, copper-nickel alloys, & inconel nickel-chromium-iron are satisfactory for dry or hot sulfur dioxide, but they are readily corroded below the dew point or by wet sulfur dioxide gas. Liquid sulfur dioxide produces serious corrosion of iron, brass, and copper at about 0.2 wt% or higher moisture content.
... Sulfur dioxide (SO2) can be produced endogenously from normal metabolism of sulfur-containing amino acids. L-cysteine is oxidized via cysteine dioxygenase to L-cysteinesulfinate, and the latter can proceed through transamination by glutamate oxaloacetate transaminase (GOT) to beta-sulfinylpyruvate which decomposes spontaneously to pyruvate and SO2 ... Endogenous production of SO2 /was detected in spontaneous hypertensive rats/ in all cardiovascular tissues, including in heart, aorta, pulmonary artery, mesenteric artery, renal artery, tail artery and the plasma SO2 content. As the key enzyme producing SO2, GOT mRNA in cardiovascular system was detected and found to be located enrichedly in endothelial cells and vascular smooth muscle cells near the endothelial layer ...
Once absorbed, sulfur dioxide appears to be metabolized rapidly to sulfate by the widely distributed enzyme sulfite oxidase. After it has been oxidized to sulfate, it becomes part of the large sulfate pool within the body. /It was reported/ relatively large differences in sulfite oxidase activity among five species: rats had the highest levels and rabbits the lowest. An inverse correlation was shown between enzyme activity and sensitivity to bisulfite toxicity. These results reflect species differences in rate of S-sulfonate formation.
IDENTIFICATION AND USE: Sulfur dioxide (SO2) is a colorless gas or liquid with a strong suffocating odor. SO2 is used as a fungicide and preservative for grapes. It is also used for the manufacture of corn syrups and molasses, in the manufacture of wine to destroy bacteria, mold, and unwanted yeasts, and for sterilization, and prevents the formation of nitrosamines in beer. SO2 is used to manufacture hydrosulfites, to bleach wood pulp and paper, to process, disinfect, and bleach food, for waste and water treatment, in metal and ore refining, and in oil refining. HUMAN STUDIES: Exposures of less than an hour to SO2 at levels above 10 ppm in air are irritating to the nose and throat, sometimes causing a choking sensation followed by nasal discharge, sneezing, coughing, and increased mucous secretion. Severe injuries of human eyes by sulfur dioxide have been produced only by liquified form. The minimum lethal human exposure is an airborne concentration of 400 ppm for 1 minute. The odor or taste is noticeable at airborne concentrations of 3 to 5 ppm, throat and conjunctival irritation and lacrimation start at 8 to 12 ppm, and symptoms become severe at 50 ppm. Other reported minimum lethal concentrations of sulfur dioxide include 3000 ppm for 5 minutes and 1000 ppm for 10 minutes. Elderly patients with asthma may be more sensitive. A 76-year-old woman with asthma died following inhalation exposure to approximately 150 ppm over a period of minutes. The frequencies of chromosomal aberrations and sister-chromatid exchange (SCE) in peripheral blood lymphocytes of 40 workers chronically exposed to SO2 at a sulfuric acid factory were studied. It was shown that the mean frequency of chromosomal aberrations and the mean frequency of lymphocytes with chromosomal aberrations of the SO2-exposed workers were both higher than controls. In human lymphocytes SO2 caused significant increases in the frequency of sister chromatid exchange and micronuclei and also induced mitotic delays and decreased mitotic index and replication index. The potential risk of low birth-weight baby might be higher in elder women exposed to SO2 during pregnancy. ANIMAL STUDIES: SO2 has been found to be endogenously generated from metabolism of sulfur-containing amino acids in mammals through transamination by aspartate aminotransferase. SO2 has physiological effects on the cardiovascular system, including vasorelaxation and cardiac function regulation. Eye irritation occurs at 6 ppm/4 hr in rabbits. After a 120-hr exposure to SO2 concentration of 1.1 ppm, guinea pigs showed proliferative interstitial pneumonia, bronchitis, and tracheitis and an increased histamine content in the lungs, while exposure to 0.06 ppm of SO2 for one month led to interstitial changes in the respiratory tract. In rats continuously exposed to SO2 for 5 months (0.7 ppm and 7.0 ppm), it increased the activity of serum cholinesterase and aspartate aminotransferase and caused morphological changes in the upper respiratory tract. Prolonged exposure of dogs to high concentrations of SO2 (200 ppm) causes a syndrome similar to human chronic bronchitis, involving chronic airway obstruction, airway inflammation, and symptoms of cough and mucus hypersecretion. In mice, fetal weight was reduced by 5% by exposure to SO2. Ossification of the sternebrae and occipital was retarded, but the incidence of malformations was not significantly increased. In rabbits, the incidence of a few minor skeletal variants was significantly increased in group exposed to SO2. SO2 increased the frequencies of chromosome aberrations and aberrant cells in mouse bone marrow in a dose-dependent manner. SO2 inhalation caused an increase of micronuclei frequencies in the polychromatic erythrocytes. SO2 caused significant, dose-dependent increases in DNA damage by inhalation exposure of mice. ECOTOXICITY STUDIES: SO2 was acutely toxic to fish. Green plants are extremely sensitive to atmospheric sulfur dioxide. Alfalfa, barley, cotton, and wheat can be injured at levels between 0.15 and 0.20 ppm, while potatoes, onions, and corn are far more resistant.
Evaluation: There is inadequate evidence for the carcinogenicity in humans of sulfur dioxide, sulfites, bisulfites and metabisulfites. There is limited evidence for the carcinogenicity in experimental animals of sulfur dioxide. There is inadequate evidence for the carcinogenicity in experimental animals of sulfites, bisulfites and metabisulfites. Overall evaluation: Sulfur dioxide, sulfites, bisulfites and metabisulfites are not classifiable as to their carcinogenicity to humans (Group 3).
来源:Hazardous Substances Data Bank (HSDB)
毒理性
致癌性证据
A4；不可归类为人类致癌物。
A4; Not classifiable as a human carcinogen.
来源:Hazardous Substances Data Bank (HSDB)
毒理性
致癌物分类
国际癌症研究机构致癌物：二氧化硫
IARC Carcinogenic Agent:Sulfur dioxide
来源:International Agency for Research on Cancer (IARC)
毒理性
致癌物分类
国际癌症研究机构（IARC）致癌物分类：第3组：无法归类其对人类致癌性
IARC Carcinogenic Classes:Group 3: Not classifiable as to its carcinogenicity to humans
来源:International Agency for Research on Cancer (IARC)
Although the major route of absorption of the relevant sulfur compounds and particulate matter into the body is through the intestinal tract, the respiratory tract is the most vulnerable area for airborne materials. Most studies on both man and animals have indicated that 40 to 90% or more of inhaled sulfur dioxide is absorbed in the upper respiratory tract. Taken into the blood stream, it appears to be widely distributed throughout the body, metabolized, and excreted via the urinary tract. The deposition pattern of particulate matter varies with particle size, shape, and density, and also with airflow conditions. Deposited particles are largely phagocytized and transported to the mucociliary escalator, into the interstitium, or to the lymphatic system. The biological half-times range from days to years depending on their chemical composition. Soluble particles may dissolve in the mucous or aqueous lining of the lungs. In the first case, they will be eliminated via the mucociliary route. In the second, they may diffuse into the lymph or blood.
Sulfur dioxide is highly soluble in aqueous media. Absorption after inhalation has been studied in rabbits and man. In rabbits, about 40% of the inhaled sulfur dioxide is absorbed in the nose and pharynx when concentrations of about 290 ug/cu m (0.1 ppm) are inhaled. At higher concentrations (29-290 mg/cu m, 10-100 ppm), the fraction absorbed is much higher (about 95%). The reasons for these different rates of absorption are not clear. In dogs, more than 99% of the inhaled sulfur dioxide is absorbed by the nose at exposure levels of 2.9-140 mg/cu m (1-50 ppm).
Sulfur dioxide is highly soluble in water and, therore, is absorbed efficiently in the upper respiratory tract. Two factors affecting the efficiency of absorption are the mode of breathing (oral versus oronasal) and ventilation rate. The nose filters out most inhaled sulfur dioxide, preventing its passage to sensitive irritant receptors at and below the larynx. At rest, most people (about 85%) breathe through the nose, providing protection against the pulmonary toxicity of sulfur dioxide. Mouth breathing, particularly at higher airflow rates, substantially increases the fraction of sulfur dioxide reaching the lung. Thus, voluntary hyperventilation or exercise at a level of exertion requiring oronasal breathing lowers the threshold for sulfur dioxide-induced respiratory symptoms and bronchomotor responsiveness. Deep lung penetration and toxicity are enhanced by oxidation and adsorption to submicrometer acidic particles.
Radiolabeled sulfur dioxide is absorbed from the respiratory tract of experimental animals in the blood and is distributed throughout the body, concentrating in the liver, spleen, esophagus, and kidneys. It is metabolized to a variety of sulfur-containing compounds and is excreted principally via the urine as sulfate. Significant quantities of sulfur dioxide may be retained for a week or more in the lungs and trachea of experimental animals.
While sulfur dioxide (SO(2)) has been previously known for its toxicological effects, it is now known to be produced endogenously in mammals from sulfur-containing amino acid L-cysteine. L-cysteine is catalyzed by cysteine dioxygenase (CDO) to L-cysteine sulfinate, which converts to beta-sulfinylpyruvate through transamination by aspartate aminotransferase (AAT), and finally spontaneously decomposes to pyruvate and SO(2). The present study explored endogenous SO(2) production, and AAT and CDO distribution in different rat tissue. SO(2) content was highest in stomach, followed by tissues in the right ventricle, left ventricle, cerebral gray matter, pancreas, lung, cerebral white matter, renal medulla, spleen, renal cortex and liver. AAT activity and AAT1 mRNA expression were highest in the left ventricle, while AAT1 protein expression was highest in the right ventricle. AAT2 and CDO mRNA expressions were both highest in liver tissue. AAT2 protein expression was highest in the renal medulla, but CDO protein expression was highest in liver tissue. In all tissues, AAT1 and AAT2 were mainly distributed in the cytoplasm rather than the nucleus. These observed differences among tissues endogenously generating SO(2) and associated enzymes are important in implicating the discovery of SO(2) as a novel endogenous signaling molecule.
Herbicidally active guanidine derivatives of the formula ##STR1## in which m represents the numbers zero, 1 or 2, R.sup.5 represents an optionally substituted radical from the series comprising alkyl, aralkyl, aryl and heteroaryl, R.sup.2 represents a pyrimidin-2-yl radical which is substituted by halogen, amino, cyano or formyl and/or by optionally substituted radicals from the series comprising alkyl, alkoxy, alkylamino, dialkylamino, alkylcarbonyl and alkoxycarbonyl, R.sup.3 represents hydrogen, an optionally substituted radical from series comprising alkyl, cycloalkyl, alkenyl, alkinyl and aralkyl, R.sup.9 represents hydrogen or optionally substituted alkyl and R.sup.10 represents an optionally substituted radical from the series comprising alkyl, alkenyl, alkinyl, cycloalkyl, aralkyl, aryl, heteroaryl, alkyl- or alkoxycarbonyl and alkyl- or arylsulphonyl, or R.sup.9 and R.sup.10 together represent alkanediyl which is optionally interrupted by an oxygen atom; and M represents hydrogen, one equivalent of a metal, or an ammonium radical which is optionally substituted by alkyl, alkenyl, alkinyl and/or aralkyl, or--in the case in which M is bonded to the same nitrogen atom as R.sup.2 --also represents an optionally substituted radical from the series comprising alkyl, alkenyl, alkinyl and aralkyl, or acid adducts thereof.
A process for the preparation of a guanidine derivative of the formula ##STR1## in which R.sup.1 represents hydrogen or the radical R.sup.5 --S(O).sub.m --, m represents the numbers zero, 1 or 2 and R.sup.5 represents an optionally substituted radical from the series comprising alkyl, aralkyl, aryl and heteroaryl, R.sup.2 represents a six-membered aromatic heterocyclic structure which contains at least one nitrogen atom and is substituted, and R.sup.8 represents an optionally substituted radical from the series comprising C.sub.1 -C.sub.6 -alkyl, alkenyl, alkinyl, cycloalkyl, phenylalkyl and aryl, which comprises reacting a guanidine derivative of the formula ##STR2## with one or two molar equivalent(s), respectively, of a halogen/sulphur compound of the formula R.sup.5 --S(O).sub.m --X.sup.1 in which X.sup.1 represents fluorine, chlorine or bromine. The compounds are herbicidally active.
A plant growth regulating compound of the formula ##STR1## in which R.sup.2 is an optionally substituted nitrogen heterocyclic radical, R.sup.3 is hydrogen, alkyl, cycloalkyl, alkenyl, alkinyl or aralkyl, and R.sup.4 is hydrogen, or if R.sup.3 is not hydrogen R.sup.4 may be hydroxyl or a variety of radicals, or R.sup.3 and R.sup.4 together may form a ring, or an acid adduct thereof.
4' SUBSTITUTED COMPOUNDS HAVING 5-HT6 RECEPTOR AFFINITY
申请人：Dunn Robert
公开号：US20080318941A1
公开（公告）日：2008-12-25
The present disclosure provides compounds having affinity for the 5-HT
6
receptor which are of the formula (I):
wherein R
1
, R
2
, R
5
, R
6
, B, D, E, G, Q, x and n are as defined herein. The disclosure also relates to methods of preparing such compounds, compositions containing such compounds, and methods of use thereof.
Compounds and uses thereof for decreasing activity of hormone-sensitive lipase
申请人：——
公开号：US20030166644A1
公开（公告）日：2003-09-04
Use of compounds to inhibit hormone-sensitive lipase, pharmaceutical compositions comprising the compounds, methods of treatment employing these compounds and compositions, and novel compounds. The present compounds are inhibitors of hormone-sensitive lipase and may be useful in the treatment and/or prevention of medical disorders where a decreased activity of hormone-sensitive lipase is desirable.
