Abstract: The effects of cyanide on the rate of respiration (oxygen-consumption) and p32 up-take were studied in rind tissue discs from root tubers of the cyanogenic plant, Manihot esculenta (cassava). The following results were obtained. 1. Cyanide (M/1000, buffered at pH 7), instead of inhibiting the rate of respiration, evoked a marked stimulation (ca 168% of control rate) of the process. Within the range of concentration tested (10-5 to 10-2 M, pH 7) Qo2 increases with cyanide concentration in a manner indicative of rate/substrate relationship. This stimulation as well as the ground rate are abolished in dead (boiled) tissues. 2. Tissue extracts made with S6rensen phosphate buffer gave an easily measurable rate of oxygen-consumption which was stimulated by cyanide to the same extent (ca. 180% of control rate) as in tissue discs. The stimulated rate as well as the ground rate of oxygen-consumption are heat labile. It appears therefore, that at least the bulk of the cyanide stimulated oxygen-consumption is located in the extractable parts of the cassava tissue and is therefore extramitochondrial. Azide (M/1000, pH 7) also stimulates tissue respiration but to a slightly lower extent than cyanide. 3. Contrary to its stimulatory effect on the rate of respiration cyanide (M/1000, pH 7) inhibits p32 uptake by cassava rind tissue discs to 70% of the control rate. This inhibition is significantly weaker than that for the same process in wheat seedlings (ca. 10% of the control rate). On the other hand p32 uptake by cassava and wheat seedlings are strongly inhibited to about the same degree (29% and 18%) by DNP the un-coupling agent for phosphorylation. It was concluded from these results that the respiration-dependent process of p32 up-take in the tissues of a cyanogenic plant (cassava), like that in other commonly investigated plant tissues, is also mediated largely through the process of oxidative phosphorylation. The bulk of the cyanide-stimulated oxygen-consumption is extra-mitochondrial. The physiological significance of this enzyme mediated stimulatory effect by cyanide was considered in the light of a detoxication mechanism.