Outcome of Cadmium on Aminergic System and Protective Function of Vitamin-C

Jyostna.V ¹ , Anuhya.G ² , Ushakiranmayi. Managamuri³ , Srinuvasulu K⁴ , Sudhakar. Poda⁵

1. Department of Biotechnology, Acharya Nagarjuna University, Nagarjuna Nagar, Guntur, India.
2. Department of Biotechnology, Acharya Nagarjuna University, Nagarjuna Nagar, Guntur, India.
3. Department of Microbiology, Acharya Nagarjuna University, Nagarjuna Nagar, Guntur, India.
4. Department of Biotechnology, K L University, Vaddeswaram, Guntur, India.
5. Department of Biotechnology, Acharya Nagarjuna University, Nagarjuna Nagar, Guntur, India.

Correspondence should be addressed to: Department of Biotechnology, Acharya Nagarjuna University, Nagarjuna Nagar, Guntur, India| Department of Biotechnology, Acharya Nagarjuna University, Nagarjuna Nagar, Guntur, India| Department of Microbiology, Acharya Nagarjuna University, Nagarjuna .

Section:Research Paper, Product Type: Isroset-Journal
Vol.5 , Issue.2 , pp.18-23, Apr-2018

CrossRef-DOI:   https://doi.org/10.26438/ijsrbs/v5i2.1823

Online published on Apr 30, 2018

Copyright © Jyostna.V, Anuhya.G, Ushakiranmayi. Managamuri, Srinuvasulu K, Sudhakar. Poda . This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
 

View this paper at   Google Scholar | DPI Digital Library

XML View     PDF Download

How to Cite this Paper

533 Views    256 Downloads    103 Downloads

Abstract :
Cadmium (Cd) is an extremely toxic metal and has a long biological half-life in humans, it enters the brain parenchyma and neurons causing neurological alterations in humans and animal models, leading to lower attention, hyper nociception, olfactory dysfunction and memory deficits. Rats were exposed to low (2mg/kg bw) and high dose (5mg/kg bw) of Cd through subcutaneous injections. The activity levels of epinephrine, norepinephrine and dopamine contents were studied in discrete brain areas of the young rats such as hippocampus, cerebral cortex and cerebellum. Hippocampal levels of catecholamines were significantly reduced in rats exposed to Cd. Our data suggest that Cd exposure disturbs aminergic system in the hippocampus, cerebral cortex and cerebellum and may contribute to the alterations in neurotransmitters.

Key-Words / Index Term :
Dopamine, Epinephrine, Norepinephrine, Cadmium, Vitamin-C

References :
[1] R. Shiman, M.Akino, S. Kaufman Solubilization and partial purification of tyrosine hydroxylase from bovine medulla. J. Biol. Cheer. 246, 1330—1340. 1971.
[2] M.Velasco, A.Lushsinger, Dopamine: Pharmacologic and Therapeutic Aspects. Am J Ther Vol 5, Issue 1, pp. 37-43. 1998.
[3] J.R.Cooper, F.E.Bloom, R.H. Roth, In the biochemical Basis of Neuropharmacology, 4th edition. Oxford University Press, New York. 1982.
[4] G.M. Jaffe Vitamin C. In: Machlin L, ed. Handbook of vitamins. New York: Marcel Dekker Inc, pp.199–244. 1984
[5] A.A.Woodall, B.N. Ames Diet and oxidative damage to DNA: the importance of ascorbate as an antioxidant. In: Packer L, Fuchs J, eds. Vitamin C in health and disease. New York: Marcel Dekker Inc, pp.193–203. 1997.
[6] M. Levine New concepts in the biology and biochemistry of ascorbic acid. N Engl J Med Vol 314, pp.892–902. 1986.
[7] C.S. Tsao An overview of ascorbic acid chemistry and biochemistry. In: Packer L, Fuchs J, eds. Vitamin C in health and disease. New York: Marcel Dekker Inc, pp25–58. 1997.
[8] B.J.Burri, R.A. Jacob Human metabolism and the requirement for vitamin C. In: Packer L, Fuchs J, eds. Vitamin C in health and disease. New York: Marcel Dekker Inc. pp.341–66. 1997.
[9] B.Halliwell Vitamin C: antioxidant or pro-oxidant in vivo. Free Radic Res. Vol25, pp. 439–54. 1996.
[10] A.Meister Glutathione-ascorbic acid antioxidant system in animals.J Biol Chem Vol 269, pp. 9397–400. 1994.
[11] H.P. Kari, P.P.Davidson, H.H. Herbert, M.H. Kochbar, Effects of Ketoamine on brain monoamine levels in rats. Res. Comm. Chem. Path. Pharamacol. Vol 20, pp. 475-488. 1978.
[12] G.B.Ansell, M.F. Beeson, A rapid and sensitive procedure for the combined assay of noradrenaline, dopamine and serotonin in a single brain sample. Anal. Biochem. Vol 23 pp. 196-206. 1968.
[13] R.J. Beninger, The role of dopamine in locomotor control. Brain Research Reviews. Vol 6, 173-196. 1983.
[14] C. Oberlander, B. Blaquière, J.F. Pujol, Distinct functions for dopamine and serotonin in locomotor behaviour: evidence using the 5-HT1 agonist RU 24969 in globus pallidus-lesioned rats. Neuroscience Letters. Vol 67, pp.113-118. 1986.
[15] M.Antonio, T.Antonio, I. Corpas, , and. M. L. Leret, Neurochemical changes in newborn rat’s brain after gestational cadmium and lead exposure. Toxicology Letters. Vol 104, Issue (1-2), pp.1–9. 1999.
[16] S.V. Chandra, K.Kalia, T. Hussain, Biogenic amines and some metals in brain of cadmium-exposed diabetic rats. J Appl Toxicol 5:378–381. 1999.
[17] L.Cahill, M.T. Alkire, Epinephrine enhancement of human memory consolidation: interaction with arousal at encoding. Neurobiol Learn Mem. Vol 79, pp.194–198. 2003.
[18] T.Moor, L.Mundorff, A. Bohringer, C. Philippsen, W.Langewitz, Reino, S.T. H. Schachinger, Evidence that baroreflex feedback influences long-term incidental visual memory in men. Neurobiol Learn Mem. Vol 84, pp.168–174. 2005.
[19] J.P.Kehrer, Free radicals as mediators of tissue injury and disease. Crit Rev Toxicol. Vol 23, Issue 1, pp.21-48. 1993
[20] L. Chen, L. Liu, S.Huang, Cadmium activates the mitogenactivated protein kinase (MAPK) pathway via induction of reactive oxygen species and inhibition of protein phosphatases 2A and 5,” Free Radical Biology and Medicine. Vol 45, Issue 7, pp1035–1044. 2008.
[21] D.Manca, A.C. Ricard, B.Trotter, G.Chevalier, , Studies of lipid peroxidation in rat tissues following administration of low and moderate doses of cadmium chloride, Toxicology Vol 67, pp. 303–323.1991.
[22] A.Shukla, G.S.Shukla, R.C. Srimal, Cadmium-induced alterations in blood brain barrier permeability and its possible correlation with decreased microvessel antioxidant potential in rat,”Human and Experimental Toxicology. Vol 15, Issue 5, pp.400– 405. 1996.
[23] H.Wieg and L. Altmann, Neurophysiology aspects of hippocampal neurotoxicity. Neurotoxicology. Vol 15, pp. 451-458. 1994.
[24] M.Gutowski, L.Altmann, K.Sveinsson, H.Weigand, Postnatal development of synaptic plasticity in the CA3 hippocampal region of control and lead exposed wistar rats. Dev. Brain. Res. Vol 98, pp. 82-90. 1997.
[25] P.Devoto, G.Flore, A. Ibba, W.Fratta, L. Pani, Lead intoxication during intrauterine life and lactation but not during adulthood reduces nucleus accumbens dopamine release as studied by brain microdialysis. Toxicol. Lett. Vol 121, pp. 199-206. 2001.
[26] H.Andersson, K.Petersson-Grave, E.Lindqvist, Low level cadmium exposure of lactating rats causes alterations in brain serotonin levels in the offspring. Neurotoxicol Teratol. Vol 19, pp.105–115. 1997.
[27] A.Bernard. Renal dysfunction induced by cadmium: biomarkers of critical effects. Biometals Vol 17, pp. 519-23. 2004.
[28] G.Nordberg K.Nogawa M,Nordberg L.Friberg Cadmium. In: Handbook on toxicology of metals.New York: Academic Press. pp. 65-78. 2007.
[29] B.Arvidson, Autoradiographic localization of cadmium in the rat brain. Neurotoxicology Vol 7 pp.89– 96. 1986.
[30] D.E.Clark, J.R.Nation, A.J. Bourgeois, M.F.Hare, D.M.Baker, E.J Hinderberger,. The regional distribution of cadmium in the brains of orally exposed adult rats. Neurotoxicology. Vol 6, 109– 14. 1985.
[31] A.Lafuente, A.Gonzalez-Carracedo, A. Romero, A.I. Esquifino, Effect of cadmium on 24-h variations in hypothalamic dopamine and serotonin metabolism in adult male rats. Exp Brain Res. Vol 6, pp. 149:200–. 2003.
[32] A.Lafuente, Marquez, N. D.Pazo, A.I. Esquifino, Effects of subchronic alternating cadmium exposure on dopamine turnover and plasma levels of prolactin, GH and ACTH. Biometals. Vol 13, pp. 47 – 55. 2000.
[33] J.C Lai,. L Lim, A.N.Davison, Differences in the inhibitory effect of Cd2+, Mn2+ and Al3+ on the uptake of dopamine by synaptosomes from forebrain and from striatum of the rat. Biochem Pharmacol. Vol 30, pp. 3123– 3135. 1981.
[34] A.H. Evans, A.J.Lees, Dopamine dysregulation syndrome in Parkinson’s disease. Curr Opin Neurol. Vol 17, Issue 393– 8. 2004.
[35] P.Remy, Y. Samson. The role of dopamine in cognition: evidence from functional imaging studies. Curr Opin Neurol. Vol 16 Issue 6, pp 37– 41. 2003.
[36] M.Paleologos, R.Cumming and R.Lazarus Cohort study of vitamin C intake and cognitive impairment. Am. J. Epidemiol. Vol 148, pp 45-50. 1998;
[37] J.Huang, D.B.Agus, C.J. Winfree, S.Kiss, W.J.Mack, R.A.McTaggart, T.F. Choudhri, L.J.Kim, J.Mocco, D.J.Pinsky, W.D.Fox, R.J.Israel, T.A., Boyd, D.W. Golde, and E.S.Connolly, Jr: Dehydroascorbic acid, a bloodbrain barrier transportable form of vitamin C, mediates potent cerebroprotection in experimental stroke. Proc Natl Acad Sci U S A Vol 98, pp.11720-11724. 2001.
[38] D.Zhang, A. Kanthasamy, Y.Yang, V.Anantharam, A. Kanthasamy. Protein kinase cd negatively regulates tyrosine hydroxylase activity and dopamine synthesis by enhancing protein phosphatase-2a activity in dopaminergic neurons. The Journal of Neuroscience. Vol 27, pp. 5349-5362. 2007.
[39] M.T. Antonio, V. Peinado, J.C. Gonza´lez, M.L Leret. Effects of maternal cadmium administration on development of monoaminergic, GABAergic and glutamatergic systems. Environ Toxicol Pharmacol Vol 29, pp. 87–90. 2010.