The consequences of a deficiency in vitamin B 1 2 for fatty acid oxidation and metabolic intermediate might accumulate should be explained. Concept Introduction: The final product of ß oxidation of fatty acids with odd number of carbon is 3-C propionyl CoA instead of acetyl CoA. Then propionyl CoA is converted into succinyl CoA via several steps. The carboxylation of a propionyl CoA to produce D-methylmalonyl CoA is the first step. The catalyst for the reaction is a biotin dependent enzyme propionyl CoA carboxylase. In the next step, D-methylmalonyl CoA so formed is isomerized into L-isomer by methylmalonyl CoA epimerase. This product is then subjected to methylmalonyl CoA mutase reaction which catalyzes the conversion of L-methylmalonyl CoA into succinyl CoA. This enzyme is vitamin B 1 2 dependent.

Question

What are some topics of interest that neurotoxicologists study? For example, toxin-induced seizures, brain death, and such along those lines?

Answer 1

Question

Chapter 23, Problem 7P

Interpretation Introduction

Interpretation:

The consequences of a deficiency in vitamin B₁₂for fatty acid oxidation and metabolic intermediate might accumulate should be explained.

Concept Introduction:

The final product of ß oxidation of fatty acids with odd number of carbon is 3-C propionyl CoA instead of acetyl CoA. Then propionyl CoA is converted into succinyl CoA via several steps.

The carboxylation of a propionyl CoA to produce D-methylmalonyl CoA is the first step. The catalyst for the reaction is a biotin dependent enzyme propionyl CoA carboxylase. In the next step, D-methylmalonyl CoA so formed is isomerized into L-isomer by methylmalonyl CoA epimerase.

This product is then subjected to methylmalonyl CoA mutase reaction which catalyzes the conversion of L-methylmalonyl CoA into succinyl CoA. This enzyme is vitamin B₁₂ dependent.

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What are some topics of interest that neurotoxicologists study? For example, toxin-induced seizures, brain death, and such along those lines?

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