English (United Kingdom)

https://curated-unify.zendy.io/wp-json/zendy-region/v1/featured_content/oa?rat=en

https://curated-unify.zendy.io/wp-json/zendy-region/v1/highlighted_journal/

Global: Zendy Plus annual

Presents the access of premium content as premium feature

Premium Content

Presents the keyphrase highlighting as premium feature

Keyphrase Highlighting

Presents the summarisation as premium feature

Summarisation

Insights

Presents the pdf analysis as premium feature

PDF Analysis

Presents the zaia usage as premium feature

ZAIA

Global: Zendy Tools annual

Global: Zendy Free Plan

Global: Zendy Tools monthly

Global: Zendy Plus monthly

Background Parkinson's disease (PD) is one of the most widespread neurodegenerative diseases. A reduction of complex I activity has been demonstrated in mitochondria of PD patients. Recently, it was shown that chronic subcutaneous exposure to low doses of rotenone (an inhibitor of mitochondrial NADH dehydrogenase and a commonly used pesticide) caused highly selective nigrostriatal dopaminergic lesions. However, while the behavioural effects of rotenone administration are well characterised, the mechanisms underlying rotenone action are unclear. Recent studies are regarding nitric oxide (NO) as universal neuronal messenger in the pathophysiology of neurodegenerative diseases. The aim of this work is to study mechanisms underlying oxidative damage of the various brain areas of rats produced by rotenone and to investigate a possible role of NO and lipid peroxidation (LPO) processes during chronic rotenone administration.

Chronic administration of rotenone induces Parkinsonian symptoms and increases levels of nitric oxide in rat brain