Abstract

Lithium (Li) therapy has widely used in the treatment of bipolar disorder. Consequently, consciousness of the side effects and pathogenesis of this metal is needed for such treatments. Recently, information on the interaction of Li with oxidative markers and organs toxicity attend the researchers over the world. In the present study we have tried to evaluate the influence of oral administration of LiCl for 4 weeks on the oxidative stress marker and histological structure of brain in male rats. Fifty adult male albino rats weighing 135±15 gm was categorized into 5 groups (10 rats each). Group I worked as negative control, group II administrated with LiCl (0.20 mg/kg bw) in drinking water, group III, IV and V were administrated with Zn (10 mg/kg bw), VE (100 mg/kg bw) and their combination twice a week besides the daily administration of LiCl for 4 weeks, respectively. Rats after anesthesia with ether killed for collocation of brain for histopathological and biochemical analysis. Data obtained showed a significant increase in LPO, NO, GSH and Li content and the activities of SOD, CAT and AChE with demylination of the nerve fibers and degeneration of neurons in brain of LiCl treated rats. Co-treatment of rats with Zn or VE results in a significant decrease in LPO, NO, GSH content in the activities of SOD, CAT and AChE with less or normal structure of the brain. However, co-treatment with combination of Zn and VE caused a significant increase in SOD, CAT and AChE activities with normal histological structure.In conclusion, the data from the present study show that Zn and VE and their interaction are effective in protection against Li- induced brain toxicity in rat with priority for the combination.

Highlights

  • Lithium is a toxic alkaline metal that occur in the environment as industrial pollution and a therapeutic use

  • Fig (1f) showed the level of AChE in brain tissue, as compared to control rats, AChE showed no significant change in Li, Li, Zn and Li, Vitamin E (VE), but it was highly significant increase in Li, Zn and VE treated groups

  • The present study showed a significant increase in LPO level in brain tissue of Li treated rats

Read more

Summary

Introduction

Lithium is a toxic alkaline metal that occur in the environment as industrial pollution and a therapeutic use. It accumulated in algae, marine animals, vegetables, rock and tobacoo leaves (Schrauzer, 2002). The dose of Li carbonate usually varies from 7-25 mg/kg per day (Allaguri et al, 2006). Prolonged Li therapy causes neuromuscular disorders (Sansone, 1985) and neuronal apoptosis in rat brain that effect on acetylcholine esterase (ACE) (Martins et al, 2008). Acetylcholine plays an important role in sending signals from one neuron to the when it is released from vesicles in the axon terminus, across the synapse, and onto receptors in the dendrites of the neuron (Habila et al, 2012)

Methods
Results
Conclusion
Full Text
Published version (Free)

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call