Fluoride Exposure Aggravates the Testicular Damage and Sperm Quality in Diabetic Mice: Protective Role of Ginseng and Banaba.

Fluoride toxicity is known to pose infertility in fluoride-intoxicated animals as well as in people residing in fluoride endemic zones. The present study addresses the degree of impairments caused due to co-exposure of high fluoride toxicity in diabetic mice. Swiss mice, Mus musculus, were subjected to fluoride toxicity by providing fluoride-supplemented drinking water (600 ppm NaF) for a period of 30 days after the confirmation of streptozotocin-induced diabetes(STZ, 50 mg/kgbw). Consequently, aggravated hyperglycemia and tissue fluoride accumulation were witnessed in fluoride-intoxicated diabetic mice; later, these toxicated mice were treated with ginseng extract (GE) and banaba leaf extract, (BLE) at dose of 150 mg/kgbw/day alone and in combination for 15 and 30-day duration to check the efficacy of phytoextracts in reversing the toxicity. The spermatological indices studied, such as sperm density, motility, viability and morphology as well as the testicular biochemical parameters showed enhanced impairment in reproductive status of fluoride-intoxicated diabetic mice. Further, 15-days administration of GE and BLE in combination at a dose of 150 mg/kgbw/day was found to be beneficial in normalizing the alterations observed upon fluoride intoxication to diabetic mice. However, the correlates showed moderate association between blood glucose levels and the spermatological as well as biochemical indices wherein the tissue fluoride levels correlate least.

Suppression of mitochondrial oxidative phosphorylation and TCA enzymes in discrete brain regions of mice exposed to high fluoride: amelioration by Panax ginseng (Ginseng) and Lagerstroemia speciosa (Banaba) extracts.

Chronic fluoride intoxication results in pathophysiological complications pertaining to soft tissues, called non-skeletal fluorosis. This study examined whether fluoride-induced alterations in selected parameters that are indicative of mitochondrial dysfunction accompany the toxic effects of fluoride in discrete brain regions in vivo and also explored the possibility of treatment with Ginseng (GE) and Banaba (BLE) either alone or with their co-exposure which is capable of reversing parameters indicative of fluoride-induced impairments in mitochondrial function. Swiss mice, Mus musculus, were given 270 ppm fluoride (600 ppm NaF) in their drinking water for 30 days, while continuing the fluoride exposure, toxicated animals were given differential doses (50-250 mg/kg body wt) of phytoextracts through oral gavage for 2 weeks. Discrete brain regions separated from dissected animals to perform biochemical assessments. Disturbances in mitochondrial enzyme complexes (I-IV) and decrements in TCA enzymes (ICDH, SDH, and aconitase) were noted in discrete brain regions upon F exposure, suggesting mitochondrial dysfunction. In addition, a significant reduction in oxidative stress indices with increased MDA content as well as decrease in reduced glutathione content and increases in catalase and SOD enzyme activity suggests the involvement of severe oxidative stress affecting the mitochondrial function(s). Treatment with either GE or BLE reversed F-induced alterations in augmenting the suppressed complex enzymes followed by TCA enzymes and oxidative stress indices in a dose independent manner. However, the co-exposure of GE and BLE at a dose of 150 mg/kgbw appeared to restore mitochondrial functioning. These results provide in vivo evidence supporting the hypothesis that fluoride induces impairments in mitochondrial function, which can be reversed by treatment with GE and BLE as well their co-exposure at 150 mg/kgbw.