Comparative Biochemistry and Physiology Part C 136 (2003) 175–180 1532-0456/03/$ - see front matter  2003 Elsevier Inc. All rights reserved. doi:10.1016/S1532-0456(03)00198-4 Catechin attenuates 6-hydroxydopamine (6-OHDA)-induced cell death in primary cultures of mesencephalic cells H.V. Nobre Junior, G.M.A. Cunha, F.D. Maia, R.A. Oliveira,M.O. Moraes, V.S.N. Rao* ´ Department of Physiology and Pharmacology, Faculty of Medicine, Federal University of Ceara, POB-3157, 60430-270, Fortaleza, CE, Brazil Received 1 May 2003; received in revised form 14 August 2003; accepted 19 August 2003 Abstract Past studies have shown the protective effects of tea catechins on oxidative cell damage induced by 6-OHDA in PC12 cells. In this study we verified whether or not catechin prevents 6-OHDA-induced oxidative cell damage in primary cultures of rat mesencephalic cells. On exposure to 6-OHDA (200 mM), the cultures showed a marked decrease in cell viability, disturbances in lipid peroxidation, and an increased generation of NO, as assayed by MTT, TBARS and nitrite assays, respectively. Introduction of catechin significantly attenuated the cell death caused by 6-OHDA at concentrations of 3.4, 34 and 340 mM in a dose-related manner. Catechin produced no marked changes on 6-OHDA-induced increases in NO, but caused a significant inhibition of lipid peroxidation. These results suggest that catechins offer similar cytoprotection against 6-OHDA-induced oxidative cell damage in mesencephalic cell cultures, as previously described in PC12 cells. The cytoprotective function of catechin results from its antioxidant property and is not due to the inhibition of nitric oxide synthase. These findings further support and substantiate traditional consumption of catechin rich greenyblack tea as protection against neurodegenerative diseases like Parkinsonism.  2003 Elsevier Inc. All rights reserved. Keywords: Catechin; Mesencephalic cell cultures; 6-Hydroxydopamine (6-OHDA); Oxidative cell damage; Lipid peroxidation; Nitric oxide (NO); Cell viability; Cytoprotection 1. Introduction The neurotoxin 6-hydroxydopamine (6-OHDA) is a commonly used tool to investigate the drugs active against human neurodegenerative conditions including Parkinson’s disease (PD). Evidence demonstrates that 6-OHDA generates reactive oxy- gen species and induces apoptosis in dopaminergic cells of rat substantia nigra (Cohen and Heikkila, 1974; Walkinshaw and Waters, 1994; He et al., 2000) through activation of caspase-3, NFkB, p53 and c-Jun transcription factors (Del Rio and Velez- *Corresponding author. Tel.: q55-85-288-8341; fax: q55- 85-288-8333. E-mail address: vietrao@ufc.br (V.S.N. Rao). Pardo, 2002). Support for this oxidative stress hypothesis for initiation of nigral dopamine neuron loss comes from the analysis of substantia nigra that has a high content of oxidizable species, including dopamine, neuromelanin, polyunsaturat- ed fatty acids and iron, and a low content of antioxidants, especially glutathione (Kidd, 2000; Carvey et al., 2001). Parkinson’s disease (PD) is the second most common neurodegenerative dis- ease which is multifactorial and associated with increased levels of oxidative stress (Ebadi et al., 2001). Antioxidants therefore may represent a novel approach for possibly halting the progression of this disease. Plant flavonoids are well known antioxidants and apart from their antioxidant capabilities they