S-allyl cysteine protects against MPTP-induced striatal and nigral oxidative neurotoxicity in mice: Participation of Nrf2. (1st February 2014)

• Record Type: Journal Article
• Authors: García, Esperanza; Santana-Martínez, Ricardo; Silva-Islas, Carlos A.; Colín-González, Ana Laura; Galván-Arzate, Sonia; Heras, Yessica; Maldonado, Perla D.; Sotelo, Julio; Santamaría, Abel
• Is Part Of: Free radical research. Volume 48:Number 2(2014:Feb.)
• Page Start: 159
• Page End: 167
• Publication Date: 2014-02-01
• Subjects: Parkinson's disease model -- dopaminergic toxicity -- oxidative stress -- MPTP -- antioxidant defense -- Nrf2 transactivation -- Phase 2 enzymes; Free radicals (Chemistry) -- Periodicals; Antioxidants -- Periodicals; Vitamin C -- Periodicals; Vitamin E -- Periodicals; 541.224
• DOI: 10.3109/10715762.2013.857019
• Languages: English
• ISSNs: 1071-5762

Abstract

Abstract: The neuroprotective properties of S-allyl cysteine (SAC) have been demonstrated in different neurotoxic paradigms, and it may be partially attributable to its antioxidant and anti-inflammatory profile. Recently, SAC has also been shown to induce neuroprotection in the rat striatum in a toxic model induced by 6-hydroxydopamine in rats through a concerted antioxidant response involving Nrf2 transcription factor nuclear transactivation and Phase 2 enzymes' upregulation. In this work, we investigated whether the SAC-induced in vivo striatal and nigral neuroprotection against 1-methyl-4-phenyl-1, 2, 3, 6-tetrahydropiridinium (MPTP) toxicity recruits Nrf2 transactivation in C57BL/6J mice. SAC (120 mg/kg, i.p. × 5 days) partially ameliorated the MPTP (30 mg/kg, i.p. × 5 days)-induced striatal and nigral dopamine and tyrosine hydroxylase depletion, attenuated the loss of Mn-SOD and HO-1 activities, and preserved the protein content of these enzymes. While no significant changes were detected for the striatal Nrf2 nuclear protein levels, the nigral Nrf2 nuclear content was decreased by MPTP and stimulated by SAC. Our findings suggest that SAC can exert neuroprotection since the origin of the dopaminergic lesion—at the substantia nigra (SN)—not only by means of direct antioxidant actions, but also through Nrf2 nuclear transactivation and Phase 2 enzymes upregulation.