Inhibition of complex I-III activity of brain mitochondria after intracerebroventricular administration of streptozotocin in rats is possibly related to loss of body weight

Abstract

The effects of streptozotocin (STZ) on the brain after intracerebroventricular (ICV) administration in rodents have been suggested to mimic the pathogenesis of sporadic Alzheimer's disease (AD). Oxidative damage, decreased glucose utilization, mitochondrial bioenergetic changes, neuroinflammation and behavioral impairment have been reported in rodents after ICV-STZ administration. However, the molecular mechanisms of STZ effects on brain after ICV administration remain highly controversial. In this study we re-examined several bioenergetic parameters of rat brain mitochondria on day 15 following ICV-STZ treatment. We observed only a moderate but statistically significant decrease in complex I-III activity in brain mitochondria from streptozotocin-treated rats. There were no changes in complex II-III activity or phosphorylation capacity of brain mitochondria after streptozotocin treatment. More importantly, it was observed that ICV-STZ treatment caused variable degrees of body-weight loss in rats, and complex I-III activity was decreased only in those rats showing a significant (more than 10%–35%) loss in body-weights.

Keywords

• Alzheimer's disease
• Cognitive deficit
• Mitochondria
• Oxidative damage
• Streptozotocin
• Neuroscience