2012, Number 2
<< Back Next >>
Arch Neurocien 2012; 17 (2)
Effect of Pb2+ on learning and memory in adult rats after a subacute exposure
Nava-Ruiz C, Méndez-Armenta M, Ríos CC
Language: Spanish
References: 37
Page: 89-95
PDF size: 134.23 Kb.
ABSTRACT
Lead (Pb
2+) is an element with no biological function in the human, and has been recognized as a dangerous
neurotoxin, even at low levels of exposure; despite efforts to reduce exposure through regulation, lead is considered
a significant public health concern. Lead is recognized by its toxic effects on several organ and systems, of particular
importance, the central nervous system. Adult population with occupational exposure present abnormalities in a
number of measures in neurobehaviour, with accumulative exposure, resulting from high blood levels; multiple
mechanisms may be involved in lead-induced neurotoxicity; one of the most important is the ability of lead to mimic
or in some cases inhibit the action of calcium (Ca
2+) as a regulator of cell function. In this work, we studied the
effect of subacute lead administration on learning and memory, as well as morphological changes in the hippocampus
of adult rats exposed. Lead acetate was given in different doses via drinking water to adult male Wistar rats for 14
days. To determine if administration of lead result in impairments in learning and memory the Morris water maze
paradigm was used, and a histopathological study to evaluate the effect of lead on hippocampal tissue. The results
in this work demonstrated that learning no was affected in any doses of lead with respect to control group, the
memory showed significative differences in high doses of lead with respect to control group, likewise, histopathological
changes in the hippocampus were observed in high doses groups with respect to control group.
REFERENCES
Tong S, Von Schirnding YE, Prapamonto T. Environmental lead exposure: a public health problem of global dimensions. Bulletin of the World Health Organization 2000; 78:1068-77.
Agency for Toxic Substance and Disease Registry (ATSDR), Toxicological Profile for Lead, U.S. Department of Health and Humans Services, Public Health Service, Centres for Diseases Control, Atlanta, GA, 2007.
Mushak P, Davis JM, Crocetti AF, Grant LD. Prenatal and postnatal ef fects of low-level lead exposure: integrated summary of a report to the US Congress on childhood lead poisoning. Environ Res 1989; 50:11-36.
Lin S, Hwang S, Marshall EG. Fertility rates among lead workers and professional bus drivers: a comparative study. Ann Epidemiol 1996; 6:201-8.
Agency for toxic substance and disease registry (ATSDR). Toxicological Profile for Lead, U.S. Department of Health and Humans Services, Public Health Service, Centres for Diseases Control, Atlanta, GA. 2005.
Bellinger CD, Bellinger MA. Childhood lead poisoning: the torturous path from science to policy. J Clin Invest 2006; 116: 853-957.
Environmental Protection Agency U.S., Air quality criteria for lead Volume I and II of II, Research Triangle Park NC: National Center for Environmental Assessment-RTO Office, 2006.
Centers for Disease Control and Prevention. Screening young children for lead poisoning: guidance for state and local public health officials. Atlanta: US Department of Health and Human Ser vices, Public Health Ser vice, CDC Childhood Lead Poisoning Prevention Program. Nov 1997.
SSA NOM-026-SSA1-1993. Criterios para evaluar la calidad del aire ambiente con respecto al plomo (Pb). Valor normado para la concentración de plomo (Pb) en el aire ambiente como medida de protección a la salud de la población. Diario Oficial de la Federación, 23 Dic. 1994.
Centers for Disease Control and Prevention. Blood lead levels- Unites States 1999-2002. MMWR 2005; 54:513-6.
White LD, Cory-Slechta DA, Gilbert ME, Tiffany-Castiglioni E, Zawia NH, Virgolini M, et al. New and evolving concepts in the neurotoxicology of lead. Toxicol Appl Pharmacol 2007;225:1-27.
Squire LR. Memory and brain. Oxford University Press, New York 1987.
Kandel ER. The molecular biology of memory storage: a dialogue between genes and synapses. Science 2001;294:1030-8.
Johnston MV, Alemi L, Harum KH. Learning, memory, and transcription factors. Pediatric Res 2003;53:369-374.
Villeda-Hernández J, Barroso-Moguel R, Méndez-Armenta M, Nava-Ruíz C,Huerta-Romero R, Rios C. Enhanced brain regional lipid peroxidation in developing rats exposed to low level lead acetate. Brain Res Bull 2001;55:247-51.
García-Arenas G, Ramírez-Amaya V, Balderas I. Cognitive deficits in adult rats by lead intoxiation are related with regional specific inhibition of cNOS. Behav Brain Res 2004;149:49-59.
Carpenter DO, Matthews MR, Parsons PJ. Long-term potentiation in the piriform cortex is blocked by lead. Cell Mol Neurobiol 1994;14:723-33.
Flores J, Albert LA. Environmental lead in Mexico, 1990-2002. Rev Environ Contam Toxicol 2004;181:37-109.
O’Dell T J, Hawkins RD, Kandel ER, Arancio O. Test of the roles of two diffusible substances in long-term potentation: Evidence for nitric oxide as a possible early retrograde messenger. Proc Natl Acad Sci USA 1991;88:11285-9.
Jett DA, Kuhlmann AC, Farmer SJ. Age-dependent effects of developmental lead exposure on performance in the Morris water maze. Pharmacol Biochem Behav 1997;57:271-9.
Kuhlmann AC, McGlothan JL, Guilarte TR. Developmental lead exposure causes spatial learning deficits in adult rats. Neurosci Lett 1997;233:101-4.
Hernández-Avila M, Romieu I, Ríos C, Rivero A, Palazuelos E. Lead-glazed ceramics as major determinations of blood lead levels in Mexican women. Environ Health Perspect 1991;94:117-20.
Rojas-López M, Santos-Burgoa C, Ríos C, Hernández-Avila M, Romieu I. Use of lead-glazed ceramics is the main factor associated with high lead in blood levels in two mexican rural communities. J Toxicol Environ Health 1994;42:45-52.
Nerad L, Ramírez A, Ormsby CE, Bermúdez R. Differential effects of anterior and posterior insular cor tex lesions on the acquisition of conditioned taste aversion and spatial learning. Neurobiol Learn Mem 1996;66:44-50.
Prados J, Trobalon JB. Locating an invisible goal in a water maze requires at least two landmarks. Psychobiology 1998;26:42-8.
Niklowitz, W. Subcellular mechanisms in lead toxicity: significance in childhood encephalopathy, neurological sequele, and late dementias. In: Rozin, L., Shiraki, H., Gréeviæ, N. (Eds.), Neurotoxicol Raven Press, New York. 1977;289-98.
Rönnbäck L, Hannson E. Chronic encephalopathies induced by mercury or lead: aspects of underlying cellular and molecular mechanisms. Br J Ind Med 1992; 49:233-40.
Tiffany-Castiglioni E. Cell culture models for lead toxicity in neuronal and glial cells. Neurotoxicol 1993;14:513-36.
Norton WT, Aquino DA, Hozumi I, Chiu FC, Brosnan CFTI. Quantitative aspects of reactive gliosis: a review. Neurochem Res 1992;17:877-85.
Norenberg MD. Reactive astrocytosis. In: Aschner M, Kimelberg HK. (Eds.), The Role of Glia in Neurotoxicity. Boca Raton CRC Press, New York, 1996, 93-107.
Van Den Berg KJ, Lammers JHCM, Hoogendijk EMG, Kulig BM. Changes in regional brain GFAP levels and behavioral functioning following subchronic lead acetate exposure in adult rats. Neurotoxicology 1996;17:725-34.
Holtzman D, DeVries C, Nguyen H, Olson J, Bensch K. Maturation of resistance to lead encephalopathy: cellular and subcellular mechanisms. Neurotoxicology 1984;5:211-25.
Stryzyñska L, Bubko I, Walski M, Rafa³owska U. Astroglial reaction during the early phase of acute lead toxicity in the adult rat brain. Toxicology 2001;165:121-31.
Zhao Y, Brandish PE, Ballou PD. A molecular basis for nitric oxide sensing by soluble guaylate cyclise. Proc Natl Acad Sci 1999;96:14753-8.
Chetty CS, Reddy GR, Murthy KS, Johnson J, Sajwan K, Desaiah D. Perinatal lead exposure alters the expression of neuronal nitric oxide synthase in rat brain. Int J Toxicol 2001;20:113-20.
Gwaltney-Brant SM. Heavy Metals. In: Handbook of toxicologic pathology. Eds. Haschek WM, Rosseaux CG, Wallig AM. Academic Press New York 2002;701-32.
Cory-Slechta DA. Relationships between lead-induced learning impairments and changes in dopaminergic, cholinergic, and glutamatergic neurotransmitter system functions. Annu Rev Pharmacol Toxicol 1995;35:391-415.