homovanillic acid/misri

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The degree of PCB chlorination determines whether the rise in urinary homovanillic acid production in rats is peripheral or central in origin.

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Commercial mixtures of polychlorinated biphenyls (PCBs, Aroclor 1016, 1254, and 1260) differing in their degree of chlorination and their accumulation in the brain were employed along with a peripheral monoamine oxidase inhibitor, debrisoquin sulfate (Declinax, DS) to determine whether the rise in

Oral dosing of rats with polychlorinated biphenyls increases urinary homovanillic acid production.

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The effect of a single oral gavage with a mixture of Aroclors 1254 and 1260 on 24-h production of urinary homovanillic acid was determined in the laboratory rat. Adult male Wistar-derived rats were exposed to a single dose of corn oil, either alone or containing equal amounts of Aroclors 1254 and

Disassociation of carbon disulfide-induced depression of flash-evoked potential peak N166 amplitude and norepinephrine levels.

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Exposure to organic solvents frequently causes functional impairment of the central nervous system (CNS). One method to examine the effects of solvent exposure on visual function is flash-evoked potentials (FEPs). Greater knowledge of the role of various neurotransmitters in generating FEP peaks

[Effects of pyrethroids on dopamine and its metabolites in nigrostriatum of male rats].

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OBJECTIVE To investigate the effects of pyrethroids on nigrostriatal dopaminergic pathways in male rats and its mechanism. METHODS Different doses of permethrin (PM, 200, 400 mg/kg) and deltamethrin (DM, 6.25, 12.50 mg/kg) in corn oil were administered to rats by gavage once daily for ten days, then

Alteration of biogenic amines in mouse brain regions by alkylating agents. I. Effects of aflatoxin B1 on brain monoamines concentrations and activities of metabolizing enzymes.

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Young adult male CD-1 mice were treated orally twice weekly for three weeks with 0, 0.05, 0.15 or 0.65 mg/kg of aflatoxin B1 (AFB1) in corn oil. Two days after the last dose, the mice were killed by decapitation and the concentrations of the brain catecholamines, norepinephrine (NE), and dopamine

Effect of repeated dietary exposure of aflatoxin B1 on brain biogenic amines and metabolites in the rat.

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Male Sprague-Dawley rats were treated po twice weekly for 3 weeks with a low (32.8 micrograms/kg) and high dose (327.9 micrograms/kg) of aflatoxin B1 (AFB1) in corn oil. A control group received corn oil only. At the end of the experiment the rats were killed, and the concentrations of the brain

Repeated developmental exposure to chlorpyrifos and methyl parathion causes persistent alterations in nicotinic acetylcholine subunit mRNA expression with chlorpyrifos altering dopamine metabolite levels.

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Organophosphates (OPs), commonly used as insecticides, inhibit acetylcholinesterase, the enzyme responsible for the inactivation of synaptic acetylcholine, which results in elevated acetylcholine neurotransmission. Nigrostriatal dopamine neurons receive substantial cholinergic innervation and

Neurobiochemical alterations induced by the artificial sweetener aspartame (NutraSweet).

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The dipeptide aspartame (NutraSweet) is a newly approved and widely used artificial sweetener in foods and beverages. Consumption of aspartame (ASM) has been reported to be responsible for neurologic and behavioral disturbances in sensitive individuals. Unfasted male CD-1 mice were dosed orally with

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