Paraquat induces oxidative stress, neuronal loss in substantia nigra region and Parkinsonism in adult rats: Neuroprotection and amelioration of symptoms by water-soluble formulation of Coenzyme Q10

Abstract

Background: Parkinson's disease, for which currently there is no cure, develops as a result of progressive loss of dopamine neurons in the brain; thus, identification of any potential therapeutic intervention for disease management is of a great importance.

Nanomicellar formulation of coenzyme Q10 (Ubisol-Q10) effectively blocks ongoing neurodegeneration in the mouse 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine model: potential use as an adjuvant treatment in Parkinson's disease

“…In cybrid cells harboring mitochondrial DNA mutations, Ubisol-Q 10 reduces the generation of ROS and prevents the tertiarybutyl hydroperoxide-induced adenosine triphosphate depletion . In vivo, it protects hippocampal pyramidal neurons from ischemia and/or reperfusion injury when delivered systemically within 30 minutes, post a 10-minute ischemic episode and in rats protects DA neurons of substantia nigra pars compacta (SNpc) from paraquat toxicity when provided prophylactically in drinking water (Somayajulu-Nitu et al, 2009). …”

Pesticides and Parkinson’s disease: A potential hazard in agricultural communities

“…The neuroprotective effect of Coenzyme Q10 has been demonstrated in both rotenone-and paraquat-induced Parkinsonian rat models. [61][62][63] In addition, Ginkgo biloba extract is neuroprotector in paraquat-induced apoptosis in vitro, 64 while acetyl-L-carnitine, sodium butyrate, vildagliptin, Hipercium perforatum, etc. had neuroprotective effects in rotenone-induced Parkinsonism in animals.…”

Toxin-Induced Parkinson’s Disease Models

“…[41][42][43][44][45] Maneb (manganese ethylene-bis-dithiocarbamate), is a contact fungicide that synergistically interacts with paraquat to markedly reduce locomotor function and increased striatal terminals and nigral neuronal damage. 46 Such synergistic interactions have been considered for the role in PD etiology and are of interest since they reflect actual human exposures. 47 Although, the toxic models reproducing PD neuropathological features have tremendously influenced our understanding of the disease, it is important to elucidate the causal relationship between toxin exposure and PD (that warrants quantitative data) since existence of methodological issues in establishing pesticide role in disease was suggested earlier.…”