Toxicology of Methyl Bromide

Yang, Raymond S. H.; Witt, Kristine L.; Alden, Charles J.; Cockerham, Lorris G.

doi:10.1007/978-1-4612-4252-9_3

Cited by 21 publications

(17 citation statements)

References 66 publications

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“…The A. purpurata oil was less effective than methyl bromide, which is able to kill S. zeamais adults with LC 50 of 0.67 mg/L (Liu and Ho, 1999). Nevertheless, methyl bromide and phosphine, the two fumigants currently used, are strongly toxic to humans (Yang et al, 1995;Nath et al, 2011). Thus, finding a natural fumigant agent from A. purpurata inflorescences for control of S. zeamais is attractive.…”

Section: Santosmentioning

confidence: 95%

Evaluation of the toxicity of essential oil from Alpinia purpurata inflorescences to Sitophilus zeamais (maize weevil)

et al. 2015

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Section: Santosmentioning

confidence: 95%

Evaluation of the toxicity of essential oil from Alpinia purpurata inflorescences to Sitophilus zeamais (maize weevil)

et al. 2015

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“…This is thought to represent a detoxification pathway of metabolism, but will also lower the antioxidant status in these organs. Methyl bromide and methyl iodide also methylate bases on DNA, with N 3 ‐methyladenine, N 7 ‐methylguanine and O 6 ‐methylguanine having been detected in the liver and lung (Bolt and Gansewendt 1993; Yang et al . 1995).…”

Section: Methylhalidesmentioning

confidence: 99%

The contributions of excitotoxicity, glutathione depletion and DNA repair in chemically induced injury to neurones: exemplified with toxic effects on cerebellar granule cells

Fonnum

Lock

2003

Journal of Neurochemistry

110

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Six chemicals, 2-halopropionic acids, thiophene, methylhalides, methylmercury, methylazoxymethanol (MAM) and trichlorfon ( Fig. 1), that cause selective necrosis to the cerebellum, in particular to cerebellar granule cells, have been reviewed. The basis for the selective toxicity to these neurones is not fully understood, but mechanisms known to contribute to the neuronal cell death are discussed. All six compounds decrease cerebral glutathione (GSH), due to conjugation with the xenobiotic, thereby reducing cellular antioxidant status and making the cells more vulnerable to reactive oxygen species. 2-Halopropionic acids and methylmercury appear to also act via an excitotoxic mechanism leading to elevated intracellular Ca 2+ , increased reactive oxygen species and ultimately impaired mitochondrial function. In contrast, the methylhalides, trichlorfon and MAM all methylate DNA and inhibit O 6 -guanine-DNA methyltransferase (OGMT), an important DNA repair enzyme. We propose that a combination of reduced antioxidant status plus excitotoxicity or DNA damage is required to cause cerebellar neuronal cell death with these chemicals. The small size of cerebellar granule cells, the unique subunit composition of their N-methyl-D-aspartate (NMDA) receptors, their low DNA repair ability, low levels of calcium-binding proteins and vulnerability during postnatal brain development and distribution of glutathione and its conjugating and metabolizing enzymes are all important factors in determining the sensitivity of cerebellar granule cells to toxic compounds.

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“…All reactions were conducted under argon or nitrogen atmosphere, unless otherwise specified. Compounds 5i , 19 5l , 20 5o and 5p 21 were previously reported.…”

Section: Methodsmentioning

confidence: 93%

An investigation of phenylthiazole antiflaviviral agents

Mayhoub

Khaliq

Botting

et al. 2011

Bioorganic & Medicinal Chemistry

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Flaviviruses are one of the most clinically important pathogens and their infection rates are increasing steadily. The phenylthiazole ring system has provided a template for the design and synthesis of antiviral agents that inhibit the flaviviruses by targeting their E-protein. Unfortunately, there is a correlation between phenylthiazole antiflaviviral activity and the presence of the reactive and therefore potentially toxic mono- or dibromomethyl moieties at thiazole-C4. Adding a linear hydrophobic tail para to the phenyl ring led to a new class of phenylthiazole antiflaviviral compounds that lack the toxic dibromomethyl moiety. This led to development of a drug-like phenylthiazole 12 that had high antiflaviviral selectivity (TI = 147).

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Toxicology of Methyl Bromide

Cited by 21 publications

References 66 publications

Evaluation of the toxicity of essential oil from Alpinia purpurata inflorescences to Sitophilus zeamais (maize weevil)

Evaluation of the toxicity of essential oil from Alpinia purpurata inflorescences to Sitophilus zeamais (maize weevil)

The contributions of excitotoxicity, glutathione depletion and DNA repair in chemically induced injury to neurones: exemplified with toxic effects on cerebellar granule cells

An investigation of phenylthiazole antiflaviviral agents

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