Objective: 

Rotenone (R), an organic and lipophilic insecticide inhibits complex-1 in electron transfer chain, upregulates superoxide, and oxidative stress-induced mitochondrial damage and cell death. Its selectivity in damaging dopaminergic neurons and potency of developing Parkinsonism like symptoms in the rat have been reported. We identified and reported the toxic effects of R in glia culture previously. Recent research has attributed neuroprotective and behavioral equilibrating serenity effects to oxytocin (ox) in addition to its well-known endocrine functions. We reported previously that ox attenuates / restores neural damage induced by diabetic neuropathy and experimental convulsions. Here, we aimed to investigate in glial culture, the trophically supportive, and neurorestorative effects of ox in general and following R toxicity, respectively.

Methods: 

Primary astroglial culture was prepared using newborn rat cortical cells. Following passagings, cells were processed in 6 groups accordingly (n=15/group; Control (C), 1 mM R, 10 nmol/L ox (ox1), 100 nmol/L ox (ox2), ox1+R and ox²⁺R; 104 cells/well x 96 wells/group). After 24 hours, cell viability was assessed using MTT method.

Results: 

Cell viability - compared to controls - decreased significantly (P<0.005) in R group, and increased significantly (P<0.05) and dose-dependently in the ox1 and ox2 groups. Moreover, cell viability – compared to R group – increased significantly (P<0.05) and dose-dependently in ox1+R and ox²⁺R groups.

Conclusions: 

Ox definitely provided trophic support for qualitative and quantitative survival of the glial cells in culture, and robustly attenuated cell damage and death rate following R toxicity. We foresee identifying and defining the site(s) and mechanism(s) of action of in-vivo and in-vitro neuroprotection induced by ox.