Augmentation of Aluminum-Induced Oxidative Stress in Rat Cerebrum by Presence of Pro-oxidant (Graded Doses of Ethanol) Exposure

被引:25
作者
Nayak, Prasunpriya [1 ,2 ]
Sharma, Shiv Bhushan [3 ]
Chowdary, Nadella Vijaya Subbaraya [2 ,4 ]
机构
[1] NRI Med Coll, Dept Physiol, Guntur 522503, AP, India
[2] Gen Hosp, Guntur 522503, AP, India
[3] Chettinad Hosp & Res Inst, Dept Physiol, Kelambakkam 603103, TN, India
[4] NRI Med Coll, Dept Biochem, Guntur 522503, AP, India
关键词
Aluminum; Cerebrum; Oxidative stress; Ethanol; LIPID-PEROXIDATION; ALZHEIMERS-DISEASE; ANTIOXIDANT SYSTEM; NEUROPROTECTIVE ROLE; N-ACETYLCYSTEINE; BRAIN; GLUTATHIONE; ACCUMULATION; HIPPOCAMPUS; INCREASES;
D O I
10.1007/s11064-010-0230-3
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Both aluminum and ethanol are pro-oxidants and neurotoxic. Considering the possibilities of co-exposure and sharing mechanisms of producing neurotoxicity, the present study was planned to identify the level of aluminum-induced oxidative stress in altered pro-oxidant (ethanol exposure) status of cerebrum. Male rats were coexposed to aluminum and ethanol for 4 weeks. After the exposure period, cerebral levels of protein, reduced glutathione (GSH), lipid peroxidation (TBARS) were measured. Activities of catalase, superoxide dismutase (SOD), glutathione reductase (GR) and glutathione perioxidase (GPx) of cerebrum were estimated. In most of the cases significant correlations were observed between the alterations and graded ethanol doses, suggesting a dose-dependency in pushing the oxidant equilibrium toward pro-oxidants. Aluminum is found to influence significantly all the studied parameters of oxidative stress. Likewise, ethanol also influenced these parameters significantly, except GR, while the interaction between ethanol and aluminum could significantly influence only the GSH content and GR activity of cerebrum. Present study demonstrate that coexposure of aluminum with pro-oxidant might favor development of aluminum-induced oxidative stress in cerebrum. This observation might be helpful in understanding of mechanism of neurodegenerative disorders and ameliorate them.
引用
收藏
页码:1681 / 1690
页数:10
相关论文
共 47 条
[1]   Regional accumulation of aluminium in the rat brain is affected by dietary vitamin E [J].
Abubakar, MG ;
Taylor, A ;
Ferns, GAA .
JOURNAL OF TRACE ELEMENTS IN MEDICINE AND BIOLOGY, 2004, 18 (01) :53-59
[2]   Lipid peroxidation facilitates aluminum accumulation in rat brain synaptosomes [J].
Amador, FC ;
Santos, MS ;
Oliveira, CR .
JOURNAL OF TOXICOLOGY AND ENVIRONMENTAL HEALTH-PART A-CURRENT ISSUES, 1999, 58 (07) :427-435
[3]   STUDIES ON ETHANOL-BRAIN CATALASE INTERACTION - EVIDENCE FOR CENTRAL ETHANOL OXIDATION [J].
ARAGON, CMG ;
STOTLAND, LM ;
AMIT, Z .
ALCOHOLISM-CLINICAL AND EXPERIMENTAL RESEARCH, 1991, 15 (02) :165-169
[4]   INCREASE IN CATALASE ACTIVITY IN DEVELOPING RAT-BRAIN CELL REAGGREGATION CULTURES IN THE PRESENCE OF ETHANOL [J].
ASPBERG, A ;
SODERBACK, M ;
TOTTMAR, O .
BIOCHEMICAL PHARMACOLOGY, 1993, 46 (10) :1873-1876
[5]   N-acetylcysteine reduced the effect of ethanol on antioxidant system in rat plasma and brain tissue [J].
Aydin, S ;
Ozaras, R ;
Uzun, H ;
Belce, A ;
Uslu, E ;
Tahan, V ;
Altug, T ;
Dumen, E ;
Senturk, H .
TOHOKU JOURNAL OF EXPERIMENTAL MEDICINE, 2002, 198 (02) :71-77
[6]   Neuroprotective role of Convolvulus pluricaulis on aluminium induced neurotoxicity in rat brain [J].
Bihaqi, Syed Waseem ;
Sharma, Meenakshi ;
Singh, Avninder Pal ;
Tiwari, Manisha .
JOURNAL OF ETHNOPHARMACOLOGY, 2009, 124 (03) :409-415
[7]  
Bondy SC, 1998, NEUROTOXICOLOGY, V19, P65
[8]   Molecular Pathogenesis of Alzheimer's Disease: Reductionist versus Expansionist Approaches [J].
Castellani, Rudy J. ;
Zhu, Xiongwei ;
Lee, Hyoung-Gon ;
Smith, Mark A. ;
Perry, George .
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES, 2009, 10 (03) :1386-1406
[9]   Oxidative stress is the primary event: Effects of ethanol consumption in brain [J].
Das S.K. ;
Hiran K.R. ;
Mukherjee S. ;
Vasudevan D.M. .
Indian Journal of Clinical Biochemistry, 2007, 22 (1) :99-104
[10]   IS ALUMINUM AN ETIOLOGIC CONTRIBUTOR TO ALCOHOLIC AMNESIA AND DEMENTIA [J].
DAVIS, WM .
MEDICAL HYPOTHESES, 1993, 41 (04) :341-343