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Kadmiyum maruziyeti spinal refleks yanıtlarının amplitüdünü arttırır

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Abstract (2. Language): 
Objective: Cadmium is an environmental pollutant and which is a potent inhibitor of voltage-dependent calcium channels. It has been shown that cadmium can causes functional disturbances in central and peripheral nervous system. In this study, it has been aimed to investigate the effects of cadmium on the spinal reflexes. Materials and Methods: pourteen, male rats were divided into two groups: Control and Cadmium. Control group animals received tap water and the rats of Cadmium group received cadmium as in the form of cadmium chloride (70 mg/L) diluted in their drinking water during the experimental period. At the end of the 60 days experimental period, the sciatic nerve was stimulated electrically with single pulses and the reflex potentials were recorded from the ipsilateral L5 ventral root. Results: After the statistical analysis, the reflex response amplitudes were significantly increased in Cadmium group in comparison to the Control group. Conclusion: Subchronic exposure to cadmium affects the rat's spinal reflex responses and extrapolation of these results to humans indicate similar possible consequences.
Abstract (Original Language): 
Amaç: Kadmiyum çevresel bir kirletici ve voltaj bağımlı kalsiyum kanallarının potent bir inhibitörüdür. Kadmiyumun santral ve periferik sinir sisteminde fonksiyonel bozukluklara neden olabileceği gösterilmiştir. Bu çalışmada kadmiyumun spinal reflekslere etkisi araştırılmıştır. Gereç ve Yöntemler: 14 adet, erkek sıçan Kontrol ve Kadmiyum grubu olarak ikiye ayrılmıştır. Kontrol grubundaki hayvanlara içme suyu, Kadmiyum grubundaki hayvanlara ise kadmiyum klorür (70 mg/L) içme suyunda çözülerek 60 gün boyunca verilmiştir. Deneysel periyodun sonunda siyatik sinir elektriksel olarak uyarılarak L5 ventral kökünden refleks potansiyelleri kaydedilmiştir. Bulgular: İstatistiksel analiz sonrasında kadmiyum grubunun refleks yanıtlarının amplitüdleri, kontrol grubuna göre istatistiksel olarak anlamlı düzeyde artmış bulunmuştur. Sonuç: Kadmiyuma subkronik maruziyet spinal refleks yanıtlarını etkiler ve insanlarda da olası benzer sonuçları düşündürür.
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REFERENCES

References: 

1. ATSDR. 1993. Agency for Toxic Substances and Disease Registry. Toxicological Profile for cadmium. Prepared under contract No. 205-88-0606 for: US Department of Health and Human Services, Public Health Service. Atlanta, GA: ATSDR.
2. Blistrabas RI, Gutman AM, Kuras AV, Mitskis A, Khusainovene NP. Effects ofcadmium ions on synaptic transmission in the frog tectum. Neurophysiology 1989; 21(6):532-539.
3. Institoris L, Papp A, Siroki O, Banerjee BD, Desi I. Immuno- and neurotoxicological investigation of combined subacute exposure with the carbamate pesticide propoxur and cadmium in rats. Toxicology 2002;178(2):161-713.
4. Chow RH. Cadmium block of squid calcium currents. Macroscopic data and a kinetic model. J Gen Physiol 1991;98(4):751-70.
5. Devi M, Fingerman M. Inhibition of acetylcholinesterase activity in the central nervous system ofthe red swamp crayfish, Procambarus clarkii, by mercury, cadmium, and lead. Bull Environ Contam Toxicol 1995;55(5):746-50.
6. Papp A, Nagymajtenyi L, Desi I. A study on electrophysiological effects of subchronic cadmium treatment in rats. Environmental Toxicology and Pharmacology 2003;13(3):181-186.
7. Yargıçoğlu P, Ağar A, Sentürk Ü, Uysal N, Kılıç D. The Effect of Pre-and Postnatal Cd Exposure on Conduction Velocity in Sciatic Nerve. Turk J Med Sci 1998; 28(1): 47-52.
8. Goering PL, Klaassen CD. Resistance to cadmium-induced hepatotoxicity in immature rats. Toxicology and Applied Pharmacology 1984:74(3):321-329.
9. Hobson M, Milhouse McD, Rajanna B. Effects of cadmium on the uptake ofdopamine and norepinephrine in rat brain synaptosomes. Bulletin of Environmental Contamination and Toxicology 1986;37: 421-426.
10. Soliakov L, Wonnacott S. Voltage-sensitive Ca2+ channels involved in nicotinic receptor-mediated [3H] dopamine release from rat striatal synaptosomes. J Neurochem 1996;67(1):163-70.
11. Yang J, Ellinor PT, Sather WA, Zhang JF, Tsien RW. Molecular determinants of Ca2+ selectivity and ion permeation in L-type Ca2+ channels. Nature 1993; 11;366(6451):158-61.
12. Taşçi N, Genç O, Bağırıcı F. The role ofL-type calcium channels in spinal reflex responses in cats. Neuroscience Research Communications 2003;33(2):124-131.
13. Molnâr G, Salânki J, Kiss T. Cadmium inhibits GABA-activated ion currents by increasing intracellular calcium level in snail neurons. Brain Research 2004;22, 1008
(2)205-211.
14. Arito H, Sudo A, Suzuki Y. Aggressive behavior of the rat induced by repeated administration ofcadmium. Toxicol Lett 1981;7(6):457-61.
15. Gonçalves JF, FiorenzaAM, Spanevello RM, Mazzanti CM, Bochi GV, Antes FG ve ark. N-acetylcysteine prevents memory deficits, the decrease in acetylcholinesterase activity and oxidative stress in rats exposed to cadmium. Chem Biol Interact 2010;186(1):53-60.
16. Gao S, Jin Y, Unverzagt FW, Ma F, Hall KS, Murrell JR ve ark. Trace element levels and cognitive function in rural elderly Chinese. J Gerontol A Biol Sci Med Sci 2008;63(6):635-41.
17. Emsley CL, Gao S, Li Y, Liang C, Ji R, Hall KS ve ark. Trace element levels in drinking water and cognitive function among elderly Chinese. Am J Epidemiol 2000, 1;151(9):913-20.

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