Xenobiotic Oxidative Phosphorylation Blockade Module

This is a mechanism module, not a specific disease. Do NOT create a "Xenobiotic Oxidative Phosphorylation Blockade" Disease entry. Disorder entries reference individual nodes via conforms_to, for example "xenobiotic_oxidative_phosphorylation_blockade#Cellular ATP Depletion despite Preserved Oxygen Delivery". Conforming nodes substitute the specific xenobiotic, the respiratory step it blocks, and the tissue in which the bioenergetic failure is expressed. Scope: the agent must act on mitochondrial ATP synthesis itself. A poison that starves tissue of oxygen before it reaches the mitochondrion belongs elsewhere, even though the endpoint looks the same. Carbon monoxide is the instructive case, because it does both: carboxyhemoglobin formation impairs oxygen delivery, which is a separate upstream mechanism, while a distinct and separately measured fraction of its toxicity is direct inhibition of cytochrome c oxidase. Only the latter arm is in scope here, so the carbon monoxide entry conforms at the respiratory-inhibition node and keeps its oxygen-delivery nodes outside this module. The blocked step is deliberately not fixed at the trigger node. Terminal oxidase inhibition, inhibition of an upstream complex, and arrest of mitochondrial protein synthesis are different lesions that converge on the same ATP deficit, and all three are in scope; the node descriptions and the conforming entry carry which one applies. Uncoupling is a fourth recognized route into the same deficit and is named in the general pharmacology cited at the trigger node, but no dismech entry currently models an uncoupler as its primary mechanism, so no conformer exercises that arm yet. The phrase "despite Preserved Oxygen Delivery" in the central effector names the feature that distinguishes this pathway from ischaemic or hypoxaemic energy failure, and it is a statement about the mechanism rather than a promise about any individual patient. A poisoned patient may be simultaneously hypotensive or hypoxaemic from another cause, and in carbon monoxide poisoning impaired delivery genuinely coexists. Read the node as asserting that a block of the respiratory chain is sufficient to produce the ATP deficit without any reduction in oxygen supply. Lactate is placed as an amplifier rather than a bare readout because the acidosis feeds back on the mechanism. The methanol observational series cited there reports formate rising well before lactate and describes the result as a self-enhancing acidotic circle, so the glycolytic shift is modelled as acting on, and not merely reporting, the downstream tissue injury. Known bundling in that same node, recorded rather than fixed: `Anaerobic Glycolytic Shift with Lactic Acidosis` carries a cellular metabolic shift and a systemic acid-base consequence together, and is tagged `ORGANISM` for the latter. Under the single-value scale discipline a node that would naturally take two values is a split signal, and this one would. It is kept whole here because the feedback the amplifier role rests on is a property of the acidosis, so splitting it without also re-pointing that edge would lose the reason the node is an amplifier at all. A later split should separate the cellular shift from the systemic acidosis and land the feedback edge on the acidosis node. Scope leakage to be aware of at the oxidative-stress node, for the same reason the carbon monoxide delivery nodes are excluded above: that entry's `Oxidative stress and free radical generation` node attributes reactive oxygen species both to mitochondrial dysfunction and to nitric oxide displaced from hemoproteins. The second route belongs to the oxygen-delivery arm this module puts outside its boundary, so the conformance carries a little of it in. The bundling predates this module and is not introduced by it; it is named here because the module's own scope paragraph is what makes it visible.