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C13 Aliphatic and Aromatic Hydrocarbons

Long-chain and branched hydrocarbons that are primary components of JP-8, include -nonanc, -dccanc, -dodccanc, -tridecane, isopropylbenzene, -propylbcnzcnc, trirnethylbenzene, -dimcthylbenzene, naphthalene, n-pentylbenzene, and -tricthylbcnzcnc. Inhaled long-chain aliphatic hydrocarbons generally show poor blood uptake because of lower blood solubility. They have relatively high lipid blood partition coefficients this can result in accumulation in lipid-rich tissues, such as brain and fat. In laboratory studies, brain concentrations of hydrocarbons and their metabolites greatly exceed their plasma concentrations. [Pg.31]

Zahlsen et al. (1993) found that C8-C10 hydrocarbons were extremely well absorbed and their tissue distribution in brain and fat were largely dependent on the number of carbon atoms. -Nonane is one component of JP-8 and it is metabolized at relatively high rates to hydroxyl derivatives, which are converted to the corresponding ketone. Other important hydrocarbons (from a [Pg.31]

Sufficiently high exposures to alkylbenzenes—such as //-diethylbenzene, -triethylbenzene, -trimethylbenzene, and isopropylbenzene—can produce adverse motor and sensory effects in rats after inhalation. Gagnaire et al. (1990) reported decreased motor and sensory conduction velocities and decreased amplitude of the sensory action potential of the tail nerve in rats exposed repeatedly to a mixture of diethylbenzene and its major metabolite, 1,2-diacetylbenzene (DAB). In the rat, 1,2-diethylbenzene was about 5 times more potent a neurotoxicant than -hexane (Gagnaire et al. 1990). Spinal-cord axonal swelling with partial demyelination has been associated with DAB exposure in rats (Kim et al. 2001). The neurotoxicity of 1,2-diethylbenzene appears to be related to formation of protein complexes reaction with amino acids of proteins to form pyrolated polymers that lead to protein cross links. [Pg.32]


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