In the lab, metabolic poisons can be used to study ATP synthesis and oxygen consumption. Many of these poisons have – or have had – other uses, from diet aids to animal poisons to antibiotics.

Poison Action
oligomycin binds to F0 and blocks the proton channel
carbon monoxide inhibits cytochrome oxidase by reacting with heme a3
trifluorocarbonylcyanide-
phenylhydrazone (FCCP) increases membrane proton permeability
antimycin prevents electron flow between cytochrome b and
cytochrome c
bongkrekic acid binds to inward‑facing site of ATP‑ADP translocase

Classify the metabolic poisons as electron transport inhibitors, uncoupling agents, ATP synthase inhibitors, or transport inhibitors.

Carbon monoxide and antimycin are classified as electron transport inhibitors, FCCP as uncoupling agent, oligomycin as ATP synthase inhibitors, and bongkrekic acid as transport inhibitor.

Explanation:

The electron transport inhibitors refers to the substances, which get combine with distinct constituents of the ETC and prevent the function of the carrier. These substances binds with the carrier and prevent its transformation, which eventually results in halting of the process. The most commonly known electron transport inhibitors are rotenone, carbon monoxide, antimycin, etc.

A molecule that prevents oxidative phosphorylation in mitochondria and prokaryotes, or photo-phosphorylation in cyanobacteria and chloroplasts by inhibiting the production of ATP is known as ATP synthase inhibitors. The most commonly known ATP synthase inhibitor is oligomycin.

Similarly to oligomycin, FCCP or trifluorocarbonylcyanide phenylhydrazone is a potent uncoupler or uncoupling agent that prevents the synthesis of ATP by enhancing membrane proton permeability.

Bongkrekic acid refers to a highly toxic transport inhibitor that prevents the ADP/ATP translocase by combining with the inward facing site of ATP-ADP translocase.

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