Short-Term in Situ Action of Melatonin on Ion Transport in Mice Kept at Restraint Stress

Melatonin, a pleiotropic hormone, is involved in many physiological functions including combating oxidative stress. However, its role in ion transport during stress response is not yet understood. The dose-dependent effect of in situ melatonin was examined in Swiss albino mice. Perfusion of melatonin at 10^-7 M for 20 minutes produced a significant decrease in Na⁺, K⁺-ATPase activity in the kidney, liver, stomach and intestinal tissues. A dose-responsive decrease in cytosolic and mitochondrial H⁺ ATPase activity was found in these tissues after melatonin perfusion. Likewise, the cytosolic and mitochondrial Ca²⁺ ATPase activities decreased in the kidney, liver, stomach and intestine. The mitochondrial Mg²⁺ ATPase activity decreased in the tested tissues in a dose-responsive manner. Subjecting mice to restraint stress for seven days increased the Na⁺, K⁺-ATPase, H⁺ ATPase, Ca²⁺ ATPase and Mg²⁺ ATPase activities to significant levels in kidney, liver, stomach and intestinal tissues. On the contrary, in-situ perfusion of melatonin to stressed mice at 10^-9 M caused decrease in the stress-induced hyperactivity of these transmembrane ion transporters. These results provide evidence for a role of melatonin in ion transporter activity and point to a protective role of melatonin in ion transport during stress response in mice.