Michel Côté

In vivo oxidation of reduced nicotinamide-adenine dinucleotide phosphate by paraquat and diquat in rat lung

Intravenous injection of rats with 156 mumol/kg of paraquat or 140 mumol/kg of diquat produced, within 60 min, a sharp drop in the ratios of NADPH to NADP in lung. The effect persisted for a time period of at least 24 h. Exposure to 100% oxygen enhanced the toxicity of both compounds without substantially amplifying changes in the NADPH/NADP ratio. Lungs retained the capability to synthesize adenine nucleotides de novo. Electron microscopic studies showed that both paraquat and diquat damage type I alveolar cells, but only paraquat produces type II cell lesions. Although bipyridylium herbicides produce acute oxidation of NADPH in vivo, there seems not to exist a straightforward relationship between this event and cell damage.

Direct observation of ultrafast long-range charge separation at polymer–fullerene heterojunctions

In polymeric semiconductors, charge carriers are polarons, which means that the excess charge deforms the molecular structure of the polymer chain that hosts it. This results in distinctive signatures in the vibrational modes of the polymer. Here, we probe polaron photogeneration dynamics at polymer:fullerene heterojunctions by monitoring its time-resolved resonance-Raman spectrum following ultrafast photoexcitation. We conclude that polarons emerge within 300 fs. Surprisingly, further structural evolution on ≲ 50-ps timescales is modest, indicating that the polymer conformation hosting nascent polarons is not significantly different from that near equilibrium. We interpret this as suggestive that charges are free from their mutual Coulomb potential because we would expect rich vibrational dynamics associated with charge-pair relaxation. We address current debates on the photocarrier generation mechanism at molecular heterojunctions, and our work is, to our knowledge, the first direct probe of molecular conformation dynamics during this fundamentally important process in these materials.

Electronic and structural properties of molecular C36

Abstract Electronic and structural properties of several isomers of molecular C 36 are investigated using the pseudopotential density functional approach. These calculations show that substitutional doping with nitrogen can lead to a 10% decrease in the C–C bond lengths of C 36 , and this effect is explained using a simple example. Further, we have calculated endohedral binding energies and demonstrate that C 36 is perhaps the smallest fullerene size which can easily trap a range of atoms. The NMR chemical shifts, evaluated for the two lowest energy fullerene isomers, show that they are sufficiently different chemically to be distinguishable experimentally.

Electron microscopy of butylated hydroxytoluene-induced lung damage in mice

Abstract This study was undertaken to analyze systematically the ultrastructural changes of the alveolar cells at several time intervals from 6 hr to 9 days following a single intraperitoneal injection (400 mg/kg) of butylated hydroxytoluene (BHT). Observation of the lung in treated mice showed ultrastructural changes in all septal cells in several focal areas. The sequence of events observed was as follows: (a) Type I epithelium was first to be damaged. From Day 1 to Day 3, this cell type exhibited alteration of cytoplasmic organelles, breaks in the plasmalemma, and a complete destruction on Days 2 and 3, leaving the basal lamina and the capillary endothelium intact. (b) After type I cells had been damaged, type II epithelium started to divide and transform themselves as early as Day 2 into a cell resembling type I in order to replace the original type I epithelium. This new cell changed its shape to become squamous, eliminated lamellar bodies, and increased the amount of ribosomes and mitochondria. Furthermore, the presence of pinocytotic vesicles and the extension of cytoplasmic processes covering the denuded basement membrane strongly suggested a type I epithelium profile. (c) Capillary endothelium showed the first signs of damage on Day 3 and Day 5. (d) Interstitial cells started to proliferate on Days 4 and 5 and invaded empty alveolar spaces. (e) Macrophages were involved from the first day and their phagocytizing activity was maximal on Day 4. The changes observed in mouse lung following BHT are therefore quite similar to other forms of lung injury produced by chemicals. BHT may be a reliable tool to study lung damage and repair.

Acute alteration of chloroform-induced hepato- and nephrotoxicity by n-hexane, methyl n-butyl ketone, and 2,5-hexanedione☆☆☆

Previous studies have suggested that administration of ketones or agents which are metabolized to ketones potentiates haloalkane toxicity in animals. To test this hypothesis, CHCl3-induced hepato- and nephrotoxicity was evaluated in male Sprague-Dawley rats pretreated with 15 mmol/kg (po) n-hexane (H), its ketonic metabolites methyl n-butyl ketone (MBK), and 2,5-hexanedione (2,5-HD) or acetone (A). Eighteen hours after pretreatment a challenging dose of CHCl3 (0.5 ml/kg, ip) was given. Liver and kidney damage were determined 24 hr later. Neither H, MBK, 2,5-HD, A, or the CHCl3 challenge dose produced marked liver or kidney injury when given alone. However, H, MBK, 2,5-HD, and A pretreatment potentiated CHCl3-induced liver and kidney injury. The ability to potentiate CHCl3-induced liver injury increased in the order of H < A < 2,5-HD ≅ MBK. The relative ranking of these chemicals in order of increasing ability to potentiate CHCl3-induced nephrotoxicity was H ≅ A < 2,5-HD ≅ MBK. These results support the concept that ketones increase the susceptibility of animals to the toxic effects of haloalkanes.

Acute alteration of chloroform-induced hepato- and nephrotoxicity by mirex and Kepone

Abstract Previous investigations have suggested that production of ketosis in laboratory animals by administration of exogenous ketones, alcohols which are metabolized to ketones, or production of diabetic ketosis potentiates halogenated hydrocarbon toxicity. To test this hypothesis, two structurally related compounds, mirex and Kepone (a ketone), were selected and their ability to modify CHCl 3 -induced hepato- and nephrotoxicity determined. Mirex (10, 50, or 250 mg/kg) or Kepone (50 mg/kg) were administered (po) to male Swiss-Webster mice. After 18 hr a challenge dose of CHCl 3 (0.1 ml/kg, po) was administered. Liver and kidney damage were determined 24 hr later, using plasma glutamic-pyruvic transaminase (GPT) and ornithine carbamyl transferase (OCT) activity, blood urea nitrogen (BUN) content, and altered renal cortical slice accumulation of p -aminohippurate (PAH) and tetraethylammonium (TEA) ion. Mirex alone did not produce signs of toxicity at any dose but produced hepatomegaly at 50 and 250 mg/kg. Kepone alone was similarly without toxic effect. CHCl 3 alone increased GPT and decreased kidney slice ion uptake. Pretreatment with mirex did not markedly alter the hepato- and nephrotoxic effects of CHCl 3 . In contrast, Kepone pretreatment potentiated CHCl 3 hepatotoxicity and may have increased CHCl 3 -induced kidney damage. These results indicate that Kepone ingestion may increase the sensitivity of the liver and kidney to CHCl 3 toxicity.

Two-dimensional spatial coherence of excitons in semicrystalline polymeric semiconductors: Effect of molecular weight

The electronic properties of macromolecular semiconductor thin films depend profoundly on their solid-state microstructure, which in turn is governed, among other things, by the processing conditions selected and the polymer chemical nature and molecular weight. Specifically, low-molecular-weight materials form crystalline domains of cofacially

Mitochondrial injury of pulmonary alveolar epithelial cells in acute paraquat intoxication

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Ab initio high-energy excitonic effects in graphite and graphene

-stacked molecules, while the usually entangled nature of higher molecular-weight polymers leads to microstructures comprised of molecularly ordered crystallites interconnected by amorphous regions. Here, we examine the interplay between extended exciton states delocalized along the polymer backbones and across polymer chains within the

Electron-phonon coupling in the C60 fullerene within the many-body GW approach

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