Format

Send to

Choose Destination
Behav Brain Res. 2006 Jul 15;171(1):9-16. Epub 2006 Apr 18.

Coenzyme Q10 modulates cognitive impairment against intracerebroventricular injection of streptozotocin in rats.

Author information

1
Neurotoxicology Laboratory, Department of Medical Elementology and Toxicology, Jamia Hamdard (Hamdard University), New Delhi, India.

Abstract

Coenzyme Q10 (CoQ10), a peculiar lipophilic antioxidant, is an essential component of the mitochondrial electron-transport chain. It is involved in the manufacturing of adenosine triphosphate (ATP) and has been linked with improving cognitive functions. The present study shows the neuroprotective effect of CoQ10 on cognitive impairments and oxidative damage in hippocampus and cerebral cortex of intracerebroventricular-streptozotocin (ICV-STZ) infused rats. Male Wistar rats (1-year old) were infused bilaterally with an ICV injection of STZ (1.5 mg/kg b.wt., in normal saline), while sham group received vehicle only. After 24 h, the rats were supplemented with CoQ10 (10 mg/kg b.wt. i.p.) for 3 weeks. The learning and memory tests were monitored 2 weeks after the lesioning. STZ-infused rats showed the loss of cognitive performance in Morris water maze and passive avoidance tests. Three weeks after the lesioning, the rats were sacrificed for estimating the contents of thiobarbituric acid reactive substances (TBARS), reduced glutathione (GSH), protein carbonyl (PC), ATP and the activities of glutathione peroxidase (GPx), glutathione reductase (GR), cholineacetyltransferase (ChAT) and acetylcholinesterase (AChE). Significant alteration in the markers of oxidative damage (TBARS, GSH, PC, GPx and GR) and a decline in the level of ATP were observed in the hippocampus and cerebral cortex of ICV-STZ rat. A significant decrease in ChAT activity and a concomitant increase in AChE activity were observed in the hippocampus. However, supplementation with CoQ10 in STZ-infused rats reversed all the parameters significantly. Thus, the study demonstrates that CoQ10 may have a therapeutic importance in the treatment of Alzheimer's type dementia.

PMID:
16621054
DOI:
10.1016/j.bbr.2006.03.009
[Indexed for MEDLINE]

Supplemental Content

Full text links

Icon for Elsevier Science
Loading ...
Support Center