Meeting Abstract
Potassium cyanide inhibits the function of the enzyme cytochrome c oxidase (aa3) in the fourth complex of the electron transport chain within the membrane of mitochondria. The binding of cyanide to aa3 prevents transport of electrons from the cytochrome c to oxygen, inhibiting the electron transport chain and preventing the cell from aerobically produce ATP. At the organismic level this causes mass death of cells within the body and leads to brain and heart failure within minutes, also known as histotoxic hypoxia. Recent studies in our laboratory and others have suggested that cyanide poisoning in cell cultures may be inhibited by simultaneous exposure to VAAM. VAAM, or vespa amino acid mixture, is a compound produced by Japanese giant hornets which has been shown to cause an increase in the production of ATP within exposed cells and an increase in overall endurance in treated house flies. Interestingly, VAAM exposure in isolation also leads to increased apoptosis and an overall increase in mortality. The experiment described here is an extension of the results gathered from work on cell cultures, in which we studied the effects of exposure to VAAM and potassium cyanide on mortality and endurance in house flies (Musca domestic.) House flies were dosed with a combination of potassium cyanide and VAAM in various time schedules, and their lifespans and endurance on swim tasks were compared to those of flies that were exposed to either cyanide or VAAM or neither (control.) Here we will discuss implications of our findings both for understanding the mechanism of action of VAAM and in interaction with mitochondrial membrane dynamics.
