Abstract:
The cerebral electrogenic Na+/K+-ATPase (sodium pump) is an important enzyme that plays a major role in the maintenance of cellular electrolyte homeostasis as well as the physiological propagation of nerve signals. In the present study, the effect of selenium dioxide (SeO2) and diphenyl diselenide (DPDS) on the transport function of the pump was investigated in vitro. Brain tissue homogenate served as the source of enzyme. The electrogenic transmembrane pump was assaulted with either SeO2 or DPDS in the absence or presence of either ATP or each of the cations (Na+ or K+). Furthermore, monothiol [glutathione (GSH) or cysteine (cys)] or dithiol [dithiothreitol (DTT)] was employed to either prevent or relieve the possible inhibition imposed by the selenium compounds. The results showed that both SeO2 and DPDS inhibited the enzyme in the absence of ATP. However, while the mono and dithiols prevented and relieved the inhibition imposed by DPDS on the activity of the enzyme, these thiols could not relieve the inhibition imposed by SeO2. More so, DPDS did not exert any inhibitory effect on the activity of the enzyme at the cationic sites whereas SeO2 evoked a concentration-dependent inhibition on the activity of the pump at these cationic sites. In addition, the thiols neither relieved nor prevented SeO2 inhibition of the pump at the cationic sites. Summarily, the present data suggested that the mechanism of inhibition of sodium pump evoked by selenium compounds maybe multifactorial. Partly, it may be associated with the chemical nature as well as the molecular volume of the selenium compounds.
