Cytochrome P-450 difference spectra. Type II interactions in insecticide-resistant and -susceptible houseflies.
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Biomedical subjects
Publications and source records attributed to R B Mailman.
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The effect of the structure of organotin compounds on their toxicity and neurotoxicity to the developing rat has been studied. Oral administration was used after selection of a vehicle that gave uniform organotin solubilization as evidenced by toxicity and chemical solubility data. This vehicle was milk plus Tween-80. Eight different organotin compounds were systematically surveyed for effects in the neonatal rat. Trimethyl- and triethyltin were most toxic, and were somewhat more toxic than tri-n-propyltin. Tri-n-butyltin was somewhat less toxic, while tricyclohexyl-, triphenyl-, diethyl- and dimethyltin were least toxic. Some higher doses of trimethyl- or triethyltin caused neuropathological changes that were characteristic for each compound, these changes being absent for the other agents. Regardless of their toxicity, significant amounts of tin, as the element, were found in brain, kidney, and liver after treatment with all agents. However, detectable blood values were only obtained for trimethyl- and triethyltin.
We examined neuroendocrine correlates of central monoamine function in patients with the generalized type of social phobia compared to healthy volunteers in order to test hypotheses of dopaminergic, noradrenergic, and/or serotonergic dysregulation in patients with this disorder. A double-blind, placebo-controlled, neuropharmacological challenge study was performed using probes for the serotonergic (fenfluramine), dopaminergic (levodopa), and noradrenergic (clonidine) systems. Twenty-one patients with DSM-III-R social phobia (generalized type) and 22 "never mentally ill" volunteers participated in the study after providing informed consent. Patients with social phobia had an augmented cortisol response to fenfluramine administration compared to the volunteers. In contrast, we found that neither the prolactin response to fenfluramine, the growth hormone or norepinephrine response to clonidine, nor the prolactin or eye-blink responses to levodopa, differed between patients with social phobia and healthy volunteers. The findings suggest that patients with social phobia may exhibit selective supersensitivity of serotonergic systems, but that dopaminergic and noradrenergic function appear normal. Further challenge studies with more specific serotonin probes before and after treatment may assist in the clarification of the pathophysiology of social phobia.