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PubMed2002

The methanol-methanolate CH(3)OH...OCH3(-) bridging ligand: tuning of exchange coupling by hydrogen bonds in dimethoxo-bridged dichromium(III) complexes.

Two bis(mu-methoxo)dichromium(III) complexes, [L(Se)(2)Cr(2)(mu-OCH(3))(2)(CH(3)OH)(2)] 1 and [L(Se)(2)Cr(2)(mu-OCH(3))(2)(CH(3)OH)(CH(3)O)](-) 2, where L(Se) represents the dianion of 2,2'-selenobis(4,6-di-tert-butylphenol), have been reported to demonstrate the effect of hydrogen bonding on the exchange coupling interactions between the chromium(III) centers. The corresponding sulfur analogue of the ligand, i.e., 2,2'-thiobis(4,6-di-tert-butylphenol), also yields the analogous [L(S)(2)Cr(2)(mu-OCH(3))(2)(CH(3)OH)(2)] 3 and [L(S)(2)Cr(2)(mu-OCH(3))(2)(CH(3)O)(CH(3)OH)](-) 4, which exhibit similar exchange coupling parameters. An acid-base dependent equilibrium between 1 and 2 or 3 and 4 has been established by electronic spectral measurements.

Journal Article↗
PubMed2004

(R,R)-Tricarbonyl[eta6-1-(diphenylphosphino)-2-[1-(diphenylphosphino)ethyl]benzene] chromium(0), (R,R)-tricarbonyl-1kappa3C-[mu1(eta6):2kappa2P,P'-1-(diphenylphosphino)-2-[1-(diphenylphosphino)ethyl]benzene][2(eta4)-norbornadiene]chromium(0)rhodium(I) tetrafluoroborate methanol 0.75-solvate and (R,R)-tricarbonyl-1kappa3C-[mu-1(eta6):2kappa2P,P'-1-(diphenylphosphino)-2-[1-(diphenylphosphino)ethyl]benzene][2(eta4)-(Z,Z)-cycloocta-1,5-diene]chromium(0)rhodium(I) tetrafluoroborate methanol 1.5-solvate.

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Journal Article↗
PubMed2005

Diaqua[N,N'-bis(5-methoxysalicylidene)ethylenediaminato-kappa(4)O,N,N',O']manganese(III) perchlorate, aqua[N,N'-bis(3,5-dichlorosalicylidene)ethylenediaminato-kappa4O,N,N',O'](methanol-kappaO)manganese(III) perchlorate and bis[mu-N,N'-bis(3-methoxysalicylidene)ethylenediaminato-kappa5O,N,N',O':O]bis[(methanol-kappaO)manganese(III)] diperchlorate.

The title compounds, a hydrogen-bonded linear chain, [Mn(C18H18N2O4)(H2O)2]ClO4, (I), a hydrogen-bonded pseudo-dimer, [Mn(C16H10Cl4N2O2)(CH4O)(H2O)]ClO4, (II), and a dimer, [Mn2(C18H18N2O4)2(CH4O)2](ClO4)2, (III), respectively, have been structurally characterized. The three complexes are completely different in their structural features, despite identical counter-anions and only slight modification of the substituents in the ligands. Complex (I) affords an elongated octahedral coordination environment, with axial Mn-O(water) distances of 2.259 (3) and 2.313 (3) A, which forms hydrogen-bonded linear chains along the crystallographic c axis. Hydrogen-bonded pseudo-dimeric compound (II) also affords an elongated octahedral coordination environment, with axial Mn-O(CH3OH) = 2.222 (3) A and Mn-O(water) = 2.266 (3) A. Dimeric complex (III) is centrosymmetric and consists of distorted octahedral Mn atoms, with axial Mn-O(CH3OH) = 2.242 (2) A and Mn-O(phenolate) = 2.348 (1) A, connected via bridging O atoms from one of the ligands. The magnetic properties of the three complexes are described.

Journal Article↗
PubMed1999

Reproductive and offspring developmental effects following maternal inhalation exposure to methanol in nonhuman primates.

INTRODUCTION: In an effort to improve air quality and decrease dependence on petroleum, the federal government, industry, and other groups have encouraged development of alternative fuels such as methanol to substitute for gasoline or diesel fuel. Methanol is also a candidate to provide the hydrogen for fuel cells, which are being developed for a variety of power sources (including motor vehicle engines). Before people are exposed to increased concentrations of methanol, the potential health effects of such exposures require study. Methanol, a simple alcohol containing one carbon atom, occurs naturally in plants and animals and participates in human metabolism. People regularly consume low doses of methanol in fruits, vegetables, and fermented beverages as well as soft drinks and foods sweetened with aspartame (which breaks down to methanol in the gastrointestinal tract). Despite its ubiquitous presence, methanol can be highly toxic if sufficient quantities are consumed. Ingestion of methanol (usually in the form of wood alcohol or tainted alcoholic beverages) can result in metabolic acidosis, blindness, and even death. Although the body has the capacity to metabolize the low doses of methanol to which people are regularly exposed, it cannot handle high doses because too much methanol overwhelms the body's ability to remove a toxic metabolite (formate). When formate accumulates, methanol poisoning occurs. One factor that regulates the rate at which formate is removed is the liver level of a derivative of the vitamin folic acid. People who are deficient in folic acid (including 15% to 30% of pregnant women) may be particularly susceptible to the toxic effects of methanol. If methanol were to be widely adopted as a fuel, environmental exposures would increase through ingestion of contaminated drinking water, inhalation of vapors from evaporative and other emissions, and dermal contact. Current concentrations of methanol in ambient air are very low, 1 to 30 parts per billion (ppb). If all motor vehicles in the United States were converted to 100% methanol fuel, methanol levels in ambient air are estimated to increase approximately 1,000-fold (to 1 to 10 ppm in cities) and in a worst-case situation could occasionally reach concentrations as high as 200 ppm in enclosed spaces (HEI 1987). Inhaling these concentrations of methanol for short periods of time is not predicted to affect formate production and thus should not present a health risk. However, little is known about the consequences of long-term inhalation of methanol vapors, especially in susceptible populations of pregnant women and developing fetuses. HEI, therefore, developed a research program to address this information gap. APPROACH: Dr. Thomas Burbacher and colleagues of the University of Washington studied the effects of long-term exposure to methanol vapors on metabolism and reproduction in adult female monkeys (Macaca fascicularis) and developmental effects in their offspring, who were exposed prenatally to methanol. The investigators exposed adult female monkeys (11 to 12 animals/group) to one of four concentrations of methanol vapors (0, 200, 600, and 1,800 ppm) for 2.5 hours a day, seven days a week during the following periods: (1) before breeding, (2) during breeding, and (3) during pregnancy. They collected blood from the adults at regular intervals to monitor methanol levels (which served as a marker of internal dose) and formate concentrations. They also conducted pharmacokinetic studies to determine whether methanol disposition (which includes absorption, distribution, metabolism, and excretion) was altered as a result of repeated methanol exposures and to assess pregnancy-related changes. Because high doses of methanol damage the central nervous system, the infants (8 to 9 animals/group) were examined at regular intervals during the first nine months of life to assess their growth and neurobehavioral development. RESULTS: Exposure to methanol vapors did n

Animals↗
PubMed1996

Maternal-fetal pharmacokinetics of methanol.

We undertook the present project to elucidate the physiologic factors that govern methanol delivery to the developing conceptus after maternal methanol exposure, and to develop a physiologically based toxicokinetic model to describe methanol disposition in pregnancy. A multi-experimental approach addressed the goals of this project. Initial experiments characterized the systemic disposition of methanol after intravenous or oral administration to nonpregnant female rats. Methanol absorption from the gastrointestinal tract was rapid (peak concentrations appeared within 1 to 2 hours after administration) and essentially complete (systemic bioavailabilities ranged from approximately 0.6 to 1.0). As anticipated for short-chain aliphatic alcohols, methanol elimination from the systemic circulation was nonlinear due to saturation of the metabolic route or routes responsible for converting methanol to formaldehyde and, ultimately, formic acid. However, a significant parallel linear route of methanol elimination was observed, which accounted for an increasingly significant fraction of total elimination as methanol doses (or systemic concentrations) increased. The disposition of methanol after oral or intravenous administration was similar in pregnant and nonpregnant female rats, regardless of the gestational stage (day 7, 14, or 20 after conception) at which the toxicokinetics of methanol were examined. This observation indicated that data from nonpregnant subjects could be used in the development of the maternal portion of a comprehensive physiologic model for methanol disposition. Parallel experiments in female mice indicated that methanol elimination was approximately twice as rapid in mice as in rats due to a significantly higher maximal velocity for methanol metabolism in the smaller rodent species. As was the case in the rat, relatively small changes in methanol elimination were observed during the course of gestation in pregnant mice. In both species, the rate of methanol metabolism by fetal liver in vitro was less than 10% that of the metabolic rate in adult liver. The kinetics of methanol delivery into the fetal environment were examined by determining amniotic fluid concentrations of methanol after intravenous administration to pregnant rats. The net rate of methanol translocation from maternal blood to amniotic fluid decreased as methanol concentration increased. Although the mechanism of this anomalous result is unknown, it possibly is due to a methanol-induced decrease in blood flow to the fetus.

Administration, Oral↗