Effect of testosterone on oxidative stress and cell damage induced by 3-nitropropionic acid in striatum of ovariectomized rats

Protective effects of epigallocatechin gallate following 3-nitropropionic acid-induced brain damage: possible nitric oxide mechanisms

“…Turan and coworkers reported that chemical preconditioning with 3-NP reduces infarct size via a mechanism that may involve increased bioavailability of NO and decreased ONOOformation (Turan et al 2006). Previous studies from different groups reported that 3-NP significantly induced oxidative damage and impaired antioxidant defense enzymes in the brain (Kumar and Kumar 2009;Kumar et al 2006Kumar et al , 2007Túnez et al 2006Túnez et al , 2007Túnez and Santamaría 2009;Pérez-De La Cruz et al 2009;Garcia et al 2008) Antioxidant drugs strategies (Curcumin, resveratrol; Kumar et al 2006Kumar et al , 2007 as well as overexpression of genes involved in attenuating oxidative stress showed a significant neuroprotective effects against 3-NP neurotoxicity (Beal et al 1995). In the present study, 3-NP significantly induced oxidative damage (increased lipid peroxidation, nitrite concentration, and depleted superoxide and catalase levels) in the striatum, cortex, and hippocampal regions.…”

Protopanaxtriol protects against 3-nitropropionic acid-induced oxidative stress in a rat model of Huntington's disease

“…In the present study, we used 3-nitropropionic acid (3-NP), a toxin produced by a number of fungal and plant species, as the model agent mimicking the characteristics of HD [5,6] . 3-NP is an irreversible inhibitor www.nature.com/aps Gao Y et al Acta Pharmacologica Sinica npg of mitochondrial succinate dehydrogenase (SDH), which has been used to explore the molecular mechanisms of cell death associated with mitochondrial dysfunction and neurodegeneration, such as in HD [7,8] ; 3-NP can significantly induce oxidative damage and impair antioxidant defense enzymes in the brain [9][10][11][12][13][14][15][16] . It has also been reported that systemic 3-NP administration leads to oxidized proteins in the striatum, as well as a massive loss of striatal neurons [16] .…”

Effects of Intramuscular or Bioadhesive Buccal Testosterone Treatment on Antioxidant Systems in Secondary Hypogonadism

“…The same group also showed increase in catalase activity after both short-and long-term incubation with gonadal steroids [29]. Testosterone was able to protect from OS and cell damage in the striatum, induced by ovariectomy (via caspase-3) and further increased by administration of 3-nitropropionic acid [30]. These studies are of fundamental importance for the investigation of neurodegenerative disorders, since OS has been implicated in the development of Alzheimer's disease, Parkinson disease and amyotrophic lateral sclerosis [31].…”