Protective effect of Wormwood extract on lead induced neurotoxicity and cognitive disorder
DOI:
https://doi.org/10.22377/ijgp.v4i3.146Abstract
Lead is a ubiquitous and a potent neurotoxicant causes several neurophysiological and behavioural alterations. Considering thevulnerability of the developing brain to Pb neurotoxicity, this study was carried out to investigate the effects of Pb exposure on brain regions acetylcholinesterase (AchE) and monoamino oxidase (MAO) enzymes activities and on behavioural changes. Wister rat were exposed to 750 ppm of lead acetate in the drinking water for 11-weeks after weaning, and treated by Artemisia Absinthium L. (wormwood) extract (200 mg.kg-1 body weight) for 4 weeks. The activities of AchE and MAO were determined in the hypothalamus, hippocampus, cortex and striatum of male rat; and general/ Locomotors activity was evaluated in the open-field test. Results indicated
a significant decrease in AchE activity in intoxicated group (Pb) compared to untreated group (as contral) (hypothalamus: -12%,
hippocampus: -57%, cerebral cortex: -18% and striatum: -43%) and in MAO activity (hypothalamus: -29%, hippocampus: -41%, cerebral cortex: -28% and striatum: -51%) respectively, with decrease crossing test score and increase sniffing test score. After, wormwood extract administration, the activity of AchE and MAO were significantly increased in all brain region compared to Pb group, but were significantly lower than control. The locomotors activity was reduced compared to Pb group. These data suggest that administration of wormwood extract for 4 weeks protect against the lead acetate-induced change in behavioural and neurobiochemical parameters
changes.
Key words: Acetylcholinesterase activity, behavioural, Brain region, Lead acetate, monoamine oxidase activity
Downloads
References
Burdette LJ, Goldstein R. Long-term behavioural and
electrophysiological changes associated with lead exposure
at different stages of brain development in the rat. Brain Res
;394:101-10.
Guilarte TR, McGlothan JL, Nihei MK. Hippocampal expression of
N-methyl-D-aspartate receptor (NMDAR1) subunit splice variant
mRNA is altered by developmental exposure to Pb(2+). Brain Res
Mol Brain Res 2000;76:299-305.
Cloues RK, Cibulsky SM, Sather WA. Ion interactions in the highaffinity
binding locus of a voltage-gated Ca2+ channel. J Gen
Physiol 2000;116:569-86.
Verina T, Rohde CA, Guilarte TR. Environmental lead exposure
during early life alters granule cell neurogenesis and morphology
in the hippocampus of young adult rats. Neuroscience 2007;145:
-47.
Flora SJ, Saxena G, Mehta A. Reversal of lead-induced neuronal
apoptosis by chelation treatment in rats: Role of ROS and
intracellular Ca2+. J Pharmacol Exp Ther 2007;322:108-16.
Nation JR, Frye GD, Van Stultz J, Bratton GR. Effects of combined
lead and cadmium exposure: Changes in schedule-controlled
responding and in dopamine, serotonin and their metabolites.
Behav Neurosci 1989;103:1108-14.
Leret ML, Garcia-Uceda F, Antonio MT. Effects of maternal lead
administration on monoaminergic, GABAergic and glutamatergic
systems. Brain Res Bull 2002;58:469-73.
Devi CB, Reddy GH, Prasanthi RPJ, Chetty CS, Reddy GR.
Developmental lead exposure alters mitochondrial monoamine
oxidase and synaptosomal catecholamine levels in rat brain. Int J
Dev Neurosci 2005;23:375-81.
Nocentini S, Guggiari M, Rouillard D, Surgis S. Exacerbating
effect of vitamin E supplementation on DNA damage induced in
cultured human normal fibroblasts by UVA radiation. Photochem
Photobiol 2001;73:370-7.
Siddique MS, Eddeb F, Mantle D, Mendelow AD. Extracts of
Ginkgo biloba and Panax ginseng protect brain proteins from free
radical induced oxidative damage in vitro. Acta Neurochir [Suppl]
;76:87-90.
Engelhart MJ, Geerlings MI, Ruitenberg A, van Swieten JC, Hofman
A, Witteman JC, et al. Dietary intake of antioxidants and risk of
Alzheimer disease. JAMA 2002;287:3223-9.
Tapiero H, Tew KD, Ba GN, Mathé G. Polyphenols: Do they
play a role in the prevention of human pathologies? Biomed
Pharmacother 2002;56:200-7.
ÄŒanadanović-Brunet JM, Ãilas SM, Ćetković G, Tumbas VT. Freeradical
scavenging activity of wormwood (Artemisia absinthium
L.) extracts. J Sci Food Agric 2005;85:265-72.
Osawa T. Protective role of dietary polyphenols in oxidative stress.
Mech Ageing Dev 1999;111:133-9.
Wiseman H, Okeily JD, Adlercreutz H, Mallet AJ, Bowery EA,
Sanders AB. Isoflavones phytoestrogen consumed in soya
decrease: F, 2, -isoprostane concentrations and increase resistance
of low-density lipoprotein to oxidation in humans. Am J Clin Nutr
;72:397-400.
Guilarte TR, McGlothan JL. Selective decrease in NR1 subunit
splice variant mRNA in the hippocampus of Pb2+-exposed rats:
Implications for synaptic targeting and cell surface expression of
NMDAR complexes. Brain Res Mol Brain Res 2003;113:37-43.
Auclair A, Drouin C, Cotecchia S, Glowinski J, Tassin JP. 5-HT2A
and alpha1b-adrenergic receptors entirely mediate dopamine
release, locomotor response and behavioural sensitization to
opiates and psychostimulants. Eur J Neurosci 2004;20:3073-84.
Glowinski J, Iversen LL. Regional studies of catecholamines in the
rat brain: I: The disposition of [3H]norepinephrine, [3H]dopamine
and [3H]dopa in various regions of the brain. J Neurochem
;13:655-69.
Green AL. Hanghton TM. A colorimetric method for the estimation
of monoamine oxidase. Biochem J 1961;78:172-5.
Ellman GL, Courtney KD, Andres V Jr, Feather-stone RM. A new
and rapid colorimetric determination of acetylcholinesterase
activity. Biochem Pharmacol 1961;7:88-95.
Azzaoui FZ, Ahami AO, Khadmaoui A. Impact of lead sub-chronic
toxicity on recognition memory and motor activity of Wistar rat.
Pak J Biol Sci 2009;12:173-7.
Trombini TV, Pedroso CG, Ponce D, Almeida AA, Godinho AF.
Developmental lead exposure in rats: Is a behavioural sequel
extended at F2 generation? Pharmacol Biochem Behav 2001;68:
-51.
Tähti H, Engelke M, Vaalavirta L. Mechanisms and models of
neurotoxicity of n-hexane and related solvents. Arch Toxicol
[Suppl] 1997;19:337-45.
Kakko I, Toimela T, Tähti H. The synaptosomal membrane bound
ATPase as a target for the neurotoxic effects of pyrethroids,
permethrin and cypermethrin. Chemosphere 2003;51:475-80.
Petit TL. Developmental effects of lead: Its mechanism in
intellectual functioning and neuralplasticity. Neurotoxicology
;7:483-96.
Silbergeld EK, Goldberg AM. Pharmacological and neurochemical
investigations of lead-induced hyperactivity. Neuropharmacology
;14:431-44.
Shih TM, Hanin I. Effect of chronic lead exposure on levels
of acetylcholine and choline. Psychopharmacology (Berlin)
;58:263-9.
Flora GJ, Seth PK. Alterations in some membrane properties in rat
brain following exposure to lead. Cytobios 2000;103:103-9.
Schwartz BS, Lee BK, Lee GS, Stewart WF, Simon D, Kelsey K, et
al. Associations of blood lead, dimercaptosuccinic acid-chelatable
lead and tibial lead with polymorphisms in the vitamin D receptor
and delta-aminalaevulinic acid dehydratase genes. Environ Health
Perspect 2000;108:949-54.
Reddy GR, Basha MR, Devi CB, Suresh A, Baker JL, Shafeek A,
et al. Lead induced effects on acetylcholinesterase activity in
cerebellum and hippocampus of developing rat. Int J Dev Neurosci
;21:347-52.
Alfano DP, Petit TL, LeBoutillier JC. Development and plasticity
of the hippocampal-cholinergic system in normal and early lead
exposed rats. Brain Res 1983;312:117-24.
Bagchi D, Vuchetich PJ, Bagchi M, Hassoun EA, Tran MX, Tang L, et al.
Induction of oxidative stress by chronic administration of sodium
dichromate [chromium VI] and cadmium chloride [cadmium II]
to rats. Free Radic Biol Med 1997;22:471-8.
Yassin Maged M. Prophylactic efficacy of crushed garlic lobes,
black seed or olive oils on cholinesterase activity in central nervous
system parts and serum of lead intoxicated rabbits. Turk J Biol
;29:173-80.
Satija NK, Vij AG. Preventive action of zinc against lead toxicity.
Indian J Physiol Pharmacol 1995;39:377-82.