A group of students of clinical nutrition were being taught about a few foods wh

Question

A group of students of clinical nutrition were being taught about a few foods which can be poisonous for the human body, if ingested in excess. These include: Almonds in raw form almonds of apricot seeds of apple and some forms of mushrooms Students were than given an assignment to find out the cause for the toxicity of these above mentioned foods. After internet searching the students came to know that these foods contain cyanide in them, and if ingested n large quantities can lead to acute cyanide poisoning. Answer the following questions on the basis of above mentioned facts: How can you relate acute cyanide poisoning with hypoxia? What would be the effects of cyanide poisoning on oxygen content and arterial pressure of oxygen. Can acute cyanide poisoning have any effects on respiration ?lf yes explain the mechanism.

Explanation / Answer

In case of cyanide poisoning, cyanide makes the body incapable to use oxygen. Cyanide lin combination with an element creates vitamin B12 which is needed for the upkeep of RBCs and nerves. The body is not able to handle rapidly largr doses of cyanide.Thus cellular absorption of oxygen is hindered and creates of hypoxia.

The arterial pressure of oxygen is normal in case of cyanide poisoning whereas the venous oxygen tension is found to be too high. This creates decreased arteriovenous oxygen difference (<10%) which results in metabolic and respiratory acidosis.

Acute cyanide poisoning inhibits cellular respiration. It impairs oxidative phosphorylation in which makes use of oxygen for the production of essential energy sources in the form of ATP. The process of transfer of electrons from NADH to oxygen via a series of electron carriers is catalyzed by cytochrome oxidase system in mitochondria. Cyanide poisoning inhibits cytochrome oxidase. It results from high binding affinity of cyanide ion with ferric ion present in the oxidised form of the enzyme. Loss of structural integrity loses the effectiveness of the enzyme. This results in inhibition of tissue utilisation of oxygen and impairment of vital functions. The rate of glycolysis is increased markedly but impaired Kreb cycle could not utilize pyruvate produced. It is then converted to lactate which is responsible for high metabolic acidosis.

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