Effect of Benzo[α］pryene and Butylated Hydroxylanisole on Learning and Memory in Rats

Yang Kai, SU Qiu-ping, QIN Qi-zhong. et al

Abstract

To investigate the neurotoxic effect of benzo［α］pryene (B［α］P) and protective effect of butylated hydroxyl anisole (BHA) on learning and memory in hippocampus of rats. Methods Ninety male SD rats were randomly divided into blank control group, solvent control group, B［α］P exposed group 〔（2 mg/（kg·d）〕, BHA group 〔50 mg/（kg·d）〕 and B［α］P+BHA combined group. Rats were given the appropriate dose oral treatment according to body mass and group (the same volume of saline and peanut oil were given to blank and solvent control group, respectively) for 90 d. After 90 d exposer, Morris water maze (MWM) was conducted to estimate rats’ learning and memory ability. The level of malonaldehyde (MDA), superoxide dismutase (SOD) activity, Na+-K+-ATPase and Ca2+-Mg2+-ATPase activity andCa2+concentration were measured after rats were sacrificed and brain tissue were removed. Results Behavioral test results showed that the escape latency of B［α］P exposed group were significantly increased than other groups (P<0.05); however, the number of crossing platform (4.13±0.78) were decreased significant. The level of MDA 〔(2.46±0.39) nmol/mg prot.〕 and Ca2+concentration〔(146.3±16.68) nmol/L〕 in the B［α］P exposed group increased significant, while the activity ofNa+-K+-ATPase and SOD 〔(76.1±11.42) nmol/mg prot.〕 were significantly decreased. Compared with B［α］P group, each index in B［α］P+BHA combined group improved significantly (P<0.05), besides, there were no statistically difference when compared with solvent control group. Conclusion The neurotoxic effect of B［α］P may be related to the decrease of ATPase activity and the increase of Ca2+concentration in hippocampus, while BHA can prevent these damages.

 

Keywords: Benzo［α］pryene, Butylated hydroxyl anisole, Oxidative stress, ATPase 

 

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References


Marta S, Bozena G, Maggalena B, et al. Factors controlling benzo(a) pyrene concentration in aerosols in the urbanized coastal zone. A case study: Gdynia* Poland (Southern Baltic Sea) . Environ Sci Pollut Res Int,2013;20(6);4154-4163.

Qi YB, Chen CZ, Tang Y, et al. The synergistic effect of benzo[ a_ pyrene and lead on learning and memory of mice. Toxicol Ind Health,2013;29(5):387-395.

Schellenberger MT, Grova N, Farinelle S, et al. Modulation of benzo[a]pyrene induced neurotoxicity in female mice actively immunized with a В a]P-diphtheria toxoid conjugate. Toxicol Appl Pharmacol. 2013; 271 (2); 175-183.

Saunders CR, Das SK . Ramesh A, et al. Benzo ( a ) pyrene- induced acute neurotoxicity in the F-344 rat; role of oxidative stress. J Appl Toxicol,2006;26(5) :427-438.

Lin X. Ni Y« Kokot S. Glassy carbon electrodes modified with gold nanoparticles for the simultaneous determination of three food antioxidants. Anal Chim Acta,2013;2(26):54-62.

Chen С, Tang Y, Jiang X, et al. Early postnatal benzo(a) pyrene exposure in Sprague-Dawley rats causes persistent neurobehavioral impairments that emerge postnatally and continue into adolescence and adulthood. Toxicol Sci.2012; 125 (1):248-261.

Hagan CE. McDevitt RA, Liu Y, et al. 5-HT ( IB ) autoreceptor regulation of serotonin transporter activity in synaptosomes. Synapse,2012;66(12); 1024-1034.

Qiu С, Cheng S, Xia Y. et al. Effects of subchronic benzo(a) pyrene exposure on neurotransmitter receptor gene expression in the rat hippocampus related with spatial learning and memory change. Toxicology,2011;289(2-3) ;83-90.

Park S, Shin H, С ho Y. Shikonin induces programmed necrosis-like cell death through the formation of receptor interacting protein 1 and 3 complex. Food Chem Toxicol.2013; 5(55) ;36-41.


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