Magnesium gluconate offers no more protection than magnesium sulphate following diffuse traumatic brain injury in rats.

Objective: Previous studies have demonstrated that magnesium salts, including the sulphate and chloride forms, are neuroprotective following traumatic brain injury (TBI). Recently, studies in cardiac ischaemia/reperfusion injury have demonstrated that the gluconate salt of magnesium may provide superior protection against oxidative damage and postischaemic dysfunction than MgSO(4). We have therefore compared the efficacy of both MgSO(4) and magnesium gluconate (MgGl(2)) on outcome following diffuse TBI in rats.

Methods: Adult male Sprague-Dawley rats were injured using the 2-metre impact acceleration model of diffuse TBI. At 30 min after injury, animals were administered with either 250 micromoles/kg i.v. MgSO(4), MgGl(2), or equal volume saline vehicle. Thereafter, animals were assessed for motor and cognitive outcome using the rotarod and Barnes maze, respectively, or their brains removed at 3 days after TBI and used for histological examination.

Results: Treatment with either magnesium salt significantly improved functional outcome as compared to vehicle treated controls. Similarly, treatment with either magnesium salt attenuated the degree of histological dark cell change at 3 days after TBI relative to the vehicle treated animals. There were no significant differences between the magnesium treated groups.

Conclusions: We conclude that MgSO(4) and MgGl(2) are equally neuroprotective following TBI. Our results suggest that MgGl(2) may only be more effective in conditions that produce ischaemia, where high concentrations of reactive oxygen species are generated.