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Biomedical subjects

B Subramanyam

Publications and source records attributed to B Subramanyam.

24 records · Page 2Linked to original sources

Toxicity of pyrethroids to Aedes aegypti larvae in relation to temperature.

The influence of temperature on the toxicity of the pyrethroids cypermethrin, permethrin, fenvalerate, d-phenothrin, flucythrinate and bioallethrin to 3rd instar Aedes aegypti larvae was determined. Based on LC50 levels, the toxicities of all pyrethroids were in the range of 1.33- to 3.63-fold greater at 20 degrees C than at 30 degrees C. Our laboratory results suggest that for larval control of Ae. aegypti, field performance of these pyrethroids may be reduced at warmer temperatures.

Aedes↗

Studies on the in vitro conversion of haloperidol to a potentially neurotoxic pyridinium metabolite.

Evidence that partially oxidized piperidine derivatives such as the Parkinsonian inducing agent 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) are biotransformed in a reaction catalyzed by monoamine oxidase B (MAO-B) to neurotoxic pyridinium metabolites led to studies resulting in the identification of the haloperidol-derived pyridinium metabolite in the urine of drug-treated rats. The present in vitro studies examine the metabolic pathway governing this overall four-electron oxidation. Although haloperidol and its 1,2,3,6-tetrahydropyridine dehydration product were not substrates for purified bovine liver MAO-B, both compounds were biotransformed to the pyridinium product by rat liver microsomal preparations. The dependence on NADPH and the inhibition by SKF-525A argue that one or more liver cytochrome P-450 isozymes may catalyze this transformation. Attempts to detect possible metabolic intermediates were not successful. Chemical model studies, however, suggest that the expected intermediary amino enol and dihydropyridinium species may be too unstable to isolate. The possible significance of this pathway with respect to haloperidol-induced central nervous system dysfunction is considered.

Animals↗

An active, aldehydic metabolite of the cell-differentiating agent hexamethylene bisacetamide.

6-Acetamidohexanal has been identified in human plasma and urine as a metabolite of the cell-differentiating agent, hexamethylene bisacetamide (HMBA). Synthesis of 6-acetamidohexanal was accomplished by oxidation of 6-acetamido-1-hexanol with pyridinium dichromate. A screen of 6-acetamidohexanal for cell-differentiating activity in HL60 human leukemia cells revealed a higher level of activity than HMBA or N-acetyl-1,6-diaminohexane, another active metabolite of HMBA. The results are consistent with a pathway which involves deacetylation of HMBA, oxidative deamination of the resulting N-acetyl-1,6-diaminohexane to yield 6-acetamidohexanal, and further oxidation to give 6-acetamidohexanoic acid.

Acetamides↗