Neuroprotective effects of mitoquinone and oleandrin on Parkinson's disease model in zebrafish.

Aim: The aim of this study is to investigate the possible protective effects of mitoquinone and oleandrin on rotenone induced Parkinson's disease in zebrafish. Materials and methods: Adult zebrafish were exposed to rotenone and mitoquinone for 30 days. Biochemical parameters were determined by spectrophotometric method and Parkinson's disease-related gene expressions were determined by reverse transcription polymerase chain reaction method. Measurement of neurotransmitters was performed by liquid chromatography tandem-mass spectrometry instrument. The accumulation of synuclein was demonstrated by immunohistochemical staining. In vitro thiazolyl blue tetrazolium bromide method was applied to determine the mitochondrial function of synaptosomal brain fractions using rotenone as a neurotoxic agent and mitoquinone and oleandrin as neuroprotective agents. Results: Mitoquinone improved the oxidant-antioxidant balance and neurotransmitter levels that were disrupted by rotenone. Mitoquinone also ameliorated the expressions of Parkinson's disease-related gene expressions that were disrupted by rotenone. According to thiazolyl blue tetrazolium bromide assay results, mitoquinone and oleandrin increased mitochondrial function which was decreased due to rotenone exposure. Conclusion: Based on the results of our study, positive effects of mitoquinone were observed in Parkinson's disease model induced by rotenone in zebrafish.

Rotenone impairs oxidant/antioxidant balance both in brain and intestines in zebrafish.

AIM OF THE STUDY: Rotenone is a commonly used pesticide that inhibits complex I of the mitochondrial electron transport system. Rotenone exposed rats demonstrate many characteristics of Parkinson Disease (PD). Oxidative stress is one of the hallmarks of PD, being the major sources of ROS in the DA neurons. In recent years the strong connection between the intestinal environment and the function of the central nervous system (CNS) has gained widespread popularity. In order to explain the mechanism underlying the GI dysfunction in PD, we aimed to investigate oxidant-antioxidant status in the brain and intestine, as well as locomotor activity, in rotenone exposed zebrafish. MATERIALS AND METHODS: Adult zebrafish were exposed to 2 mg/L rotenone for 30 days. At the end of the experiment, locomotor activity was determined by simple observation. Lipid peroxidation (LPO), nitric oxide (NO) levels, superoxide dismutase (SOD), catalase (CAT) and glutathione-S-transferase (GST) activities were determined in the homogenates. RESULTS: Locomotor activity decreased in the rotenone exposed zebrafish. LPO increased in both brain and intestines whereas NO increased only in the brain. Decreased GST and CAT activities were found in both tissues whereas SOD activity decreased only in the intestines. CONCLUSION: As a conclusion, the results of our study support the connection between gut and brain axis in rotenone exposed zebrafish by means of oxidative stress and NO for the first time in literature.