Protective effect of Bacopa monniera on methyl mercury-induced oxidative stress in cerebellum of rats

Abstract

Methyl mercury (MeHg) is a ubiquitous environmental pollutant leading to neurological and developmental deficits in animals and human beings. Bacopa monniera (BM) is a perennial herb and is used as a nerve tonic in Ayurveda, a traditional medicine system in India. The objective of the present study was to investigate whether Bacopa monniera extract (BME) could potentially inhibit MeHg-induced toxicity in the cerebellum of rat brain. Male Wistar rats were administered with MeHg orally at a dose of 5 mg/kg b.w. for 21 days. Experimental rats were given MeHg and also administered with BME (40 mg/kg, orally) for 21 days. After the treatment period, we observed that MeHg exposure significantly inhibited the activities of superoxide dismutase, catalase, glutathione peroxidase, and increased the glutathione reductase activity in cerebellum. It was also found that the level of thiobarbituric acid-reactive substances was increased with the concomitant decrease in the glutathione level in MeHg-induced rats. These alterations were prevented by the administration of BME. Behavioral interference in the MeHg-exposed animals was evident through a marked deficit in the motor performance in the rotarod task, which was completely recovered to control the levels by BME administration. The total mercury content in the cerebellum of MeHg-induced rats was also increased which was measured by atomic absorption spectrometry. The levels of NO(2) (-) and NO(3) (-) in the serum were found to be significantly increased in the MeHg-induced rats, whereas treatment with BME significantly decreased their levels in serum to near normal when compared to MeHg-induced rats. These findings strongly implicate that BM has potential to protect brain from oxidative damage resulting from MeHg-induced neurotoxicity in rat.

Fig. 1

Concentration of mercury in the cerebellum of control and experimental rats. Data represent mean ± SD of six rats in each group. *p < 0.05 significantly different from control group, using one-way ANOVA with Tukey’s post hoc test. Concentration of mercury expressed as μg/g tissue

Fig. 2

Effect of BME on the levels of TBARS, protein carbonyls, and GSH in the cerebellum of control and experimental rats. Data represent mean ± SD of six rats in each group. TBARS units expressed as μmoles of TBARS/mg protein. Protein carbonyls units expressed as nmoles/mg protein. GSH units expressed as μM/mg protein. *p < 0.05 significantly different from control group; ** p < 0.01 significantly different from MeHg-treated group, using one-way ANOVA with Tukey’s post hoc test. TBARS thiobarbituric acid-reactive substances, GSH reduced glutathione

Fig. 3

Effect of BME on the activities of GPx and GR in the cerebellum of control and experimental rats. Data represent mean ± SD of six rats in each group. GPx units expressed as μg/min/mg protein. GR units expressed as nmol NADPH oxidized/min/mg protein. *p < 0.05 significantly different from control group; ** p < 0.01 significantly different from MeHg-treated group, using one-way ANOVA with Tukey’s post hoc test. GPx glutathione peroxidase, GR glutathione reductase

Fig. 4

Effect of BME on the activities of SOD and CAT in the cerebellum of control and experimental rats. Data represent mean ± SD of six rats in each group. SOD units expressed as enzyme activity to inhibit 50% of pyrogallol auto-oxidation. CAT units expressed as nmol of H₂O₂ reduced/min/mg protein. *p < 0.05 significantly different from control group; **p < 0.01 significantly different from MeHg-treated group, using one-way ANOVA with Tukey’s post hoc test. SOD superoxide dismutase, CAT catalase

Fig. 5

Effect of BME in the NO₂ ⁻ level in serum of control and experimental rats. Data represent mean ± SD of six rats in each group. *p < 0.05 significantly different from control group; **p < 0.01 significantly different from MeHg-treated group, using one-way ANOVA with Tukey’s post hoc test. NO₂ ⁻ level expressed in μM

Fig. 6

Effect of BME in the NO₃ ⁻ level in serum of control and experimental rats. Data represent mean ± SD of six rats in each group. *p < 0.05 significantly different from control group; **p < 0.01 significantly different from MeHg-treated group, using one-way ANOVA with Tukey’s post hoc test. NO₃ ⁻ level expressed in μM