Đánh giá Stress Oxy Hóa ở Vùng Hồi Hải Mã, Tiểu Não và Vỏ Não Trước ở Chuột Con Bị Phơi Nhiễm Chì (Pb) Trong Các Thời Kỳ Cụ Thể Của Sự Phát Triển Não Bộ Ban Đầu

Biological Trace Element Research - Tập 164 - Trang 212-218 - 2015
Rajashekar Rao Barkur1, Laxminarayana Kurady Bairy2
1Department of Biochemistry, Melaka Manipal Medical College, Manipal University, Manipal, India
2Department of Pharmacology, Kasturba Medical College, Manipal University, Manipal, India

Tóm tắt

Các nghiên cứu dịch tễ học ở trẻ em đã chứng minh rằng việc tiếp xúc với chì (Pb) gây ra các khuyết tật về chức năng thần kinh và nhận thức. Nghiên cứu hiện tại đánh giá stress oxy hóa vào ngày 30 sau sinh, trong hồi hải mã, tiểu não và vỏ não trước của chuột con bị phơi nhiễm Pb trong các khoảng thời gian cụ thể của sự phát triển não bộ ban đầu. Năm nhóm chuột con đã được điều tra, và 0,2% acetate chì trong nước uống là liều lượng sử dụng. (i) Nhóm thai kỳ và cho con bú (GL) (n = 9) của chuột con bị phơi nhiễm Pb trong suốt thai kỳ và cho con bú thông qua mẹ của chúng, (ii) nhóm thai kỳ (G) (n = 9) của chuột con bị phơi nhiễm Pb chỉ trong thai kỳ, (iii) nhóm cho con bú (L) (n = 9) của chuột con bị phơi nhiễm Pb chỉ trong giai đoạn cho con bú, (iv) nhóm trước thai kỳ (PG) (n = 9) của chuột con sinh ra từ những mẹ đã tiếp xúc với Pb trong 1 tháng trước khi thụ thai, và (v) nhóm chứng bình thường (NC) (n = 9) của chuột con không bị phơi nhiễm Pb trong thời gian thai kỳ và cho con bú. Từ nghiên cứu hiện tại, rõ ràng rằng việc phơi nhiễm Pb trong các giai đoạn khác nhau của sự phát triển não bộ ban đầu (các nhóm GL, G, L và PG) gây ra stress oxy hóa và thời kỳ cho con bú (thời kỳ sau sinh) của việc phơi nhiễm Pb tạo ra stress oxy hóa tối đa.

Từ khóa

#chì (Pb) #stress oxy hóa #phát triển não bộ #chuột con #hồi hải mã #tiểu não #vỏ não trước

Tài liệu tham khảo

Yiin SJ, Lin TH (1995) Lead-catalyzed peroxidation of essential unsaturated fatty acid. Biol Trace Elem Res 50:167–172 Adegbesan BO, Adenuga GA (2007) Effect of lead exposure on liver lipid peroxidative and antioxidant defense systems of protein-undernourished rats. Biol Trace Elem Res 116:219–225 Bokara KK, Brown E, McCormick R et al (2008) Lead-induced increase in antioxidant enzymes and lipid peroxidation products in developing rat brain. Biometals 21:9–16 Adonaylo VN, Oteiza PI (1999) Lead intoxication: antioxidant defenses and oxidative damage in rat brain. Toxicology 135:77–85 Weisbrot-Lefkowitz M, Reuhl K, Perry B, Chan PH, Inouye M, Mirochnitchenko O (1998) Overexpression of human glutathione peroxidase protects transgenic mice against focal cerebral ischemia/reperfusion damage. Mol Brain Res 53:333–338 Steullet P, Cabungcal JH, Kulak A et al (2010) Redox dysregulation affects the ventral but not dorsal hippocampus: impairment of parvalbumin neurons, gamma oscillations, and related behaviors. J Neurosci 30:2547–2558 Lidsky TI, Schneider JS (2003) Lead neurotoxicity in children: basic mechanisms and clinical correlates. Brain 126:5–19 Goyer RA (1990) Transplacental transport of lead. Environ Health Perspect 89:101–105 Lataillade GP, Thoreux-Manlay A, Coffigny H, Masse R, Soufir JC (1995) Reproductive toxicity of chronic lead exposure in male and female mice. Hum Exp Toxicol 14:872–878 Namihira D, Saldivar N, Pustilnik N, Carreon GJ, Salinas ME (1993) Lead in human blood and milk from nursing women living near a smelter in Mexico city. J Toxicol Environ Health 388:225–232 Hallen PI, Jorhem L, Oskarsson A (1995) Placental and lactational transfer of lead in rats: a study of the lactational process and effects on offspring. Arch Toxicol 69:596–602 Needleman HL (1993) The current status of childhood low-level lead toxicity. Neurotoxicology 14:161–166 Markowitz M (2000) Lead poisoning: a disease for the next millennium. Curr Probl Pediatr 30:62–70 Gurer H, Ozgunes H, Neal R et al (1998) Antioxidant effects of N-acetylcysteine and succimer in red blood cells from lead-exposed rats. Toxicology 128:181–189 Lu X, Jin C, Yang J et al (2013) Prenatal and lactational lead exposure enhanced oxidative stress and altered apoptosis status in offspring rats' hippocampus. Biol Trace Elem Res 151(1):75–84 Muller RU, Bostock E, Taube JS, Kubie JL (1994) On the directional firing properties of hippocampal place cells. J Neurosci 14(12):7235–7251 Hayman R, Verriotis MA, Jovalekic A, Fenton AA, Jeffery KJ (2011) Anisotropic encoding of three-dimensional space by place cells and grid cells. Nat Neurosci 14(9):1182–1188 Holdstock JS, Mayes AR, Roberts N et al (2002) Under what conditions is recognition spared relative to recall after selective hippocampal damage in humans? Hippocampus 12:341–351 Griffiths D, Dickinson A, Clayton N (1999) Episodic memory: what can animals remember about their past? Trends Cogn Sci 3:74–80 Tulving E, Markowitsch HJ (1998) Episodic and declarative memory: a role of the hippocampus. Hippocampus 8:198–204 Raymond JL, Lisberger SG, Mauk MD (1996) The cerebellum: a neural learning machine? Science 272:1126–1131 Andreasen NC, Nopoulos P, O’Leary DS, Miller DD, Wassink T, Flaum M (1999) Defining the phenotype of schizophrenia: cognitive dysmetria and its neural mechanisms. Biol Psychiat 46(7):908–920 Schmahmann JD (2004) Disorders of the cerebellum: ataxia, dysmetria of thought, and the cerebellar cognitive affective syndrome. J Neuropsychiatry Clin Neurosci 16(3):367–378 Kolb B (1990) Animal models for human PFC-related disorders. Prog Brain Res 85:501–519 Stuss DT, Alexander MP (2000) Executive functions and the frontal lobes: a conceptual view. Psychol Res 63:289–298 Winocur G, Moscovitch M (1999) Anterograde and retrograde amnesia after lesions to frontal cortex in rats. J Neurosci 19(21):9611–9617 Moreira EG, Rosa GJ, Barros SB, Vassilieff VS, Vassillieff I (2001) Antioxidant defense in rat brain regions after developmental lead exposure. Toxicology 169(2):145–151 Verma SK, Dua R, Gill KD (2006) Impaired energy metabolism after co-exposure to lead and ethanol. Basic Clin Pharmacol Toxicol 96(6):475–479 Barkur RR, Bairy LK (2014) Histological study on hippocampus, amygdala and cerebellum following low lead exposure during prenatal and postnatal brain development in rats. Toxicol Ind Health. doi:10.1177/0748233714545624 Jaako-Movits K, Zharkovsky T, Romantchik O et al (2005) Developmental lead exposure impairs contextual fear conditioning and reduces adult hippocampal neurogenesis in the rat brain. Int J Dev Neurosci 23:627–635 Heidmets LT, Zharkovsky T, Jurgenson M, Jaako-Movits K, Zharkovsky A (2006) Early postnatal, low-level lead exposure increases the number of PSA-NCAM expressing cells in the dentate gyrus of adult rat hippocampus. Neurotoxicology 27:39–43 Chen HH, Ma T, Paul IA, Spencer JL, Ho IK (1997) Developmental lead exposure and two-way active avoidance training alter the distribution of protein kinase C activity in the rat hippocampus. Neurochem Res 22:1119–1125 Glowinski J, Iverson LL (1966) Regional studies of catecholamines in the rat brain. The deposition of [3H]norepinephrine, [3H]dopamine, and [3H]dopa in various regions of the brain. J Neurochem 13(8):655–669 Ohkawa H, Ohishi N, Yagi K (1979) Assay for lipid peroxides in animal tissues by thiobarbituric acid reaction. Anal Biochem 95:351–358 Wendel A (1981) Glutathione peroxidase. In: Jakoly WB (ed) Methods in enzymology, vol 7. Academic, New York, pp 325–333 Beutler E, Duron O, Kelly BM (1963) Improved method for the determination of blood glutathione. J Lab Clin Med 61:882–888 Lowry OH, Rosebrough NJ, Farr AL, Randall RJ (1951) Protein measurement with the Folin phenol reagent. J Biol Chem 193:265–275 Kuruvilla A, Pillay VV, Venkatesh T et al (2004) Portable lead analyzer to locate source of lead. Indian J Pediat 71:495–499 Quinlan GJ, Halliwell B, Moorhouse CP, Gutteridge JMC (1988) Action of lead(II) and aluminium(III) ions on iron-stimulated lipid peroxidation in liposomes, erythrocytes and rat liver microsomal fractions. Biochim Biophys Acta 962:196–200 Zhao Y, Wang L, Shen HB, Wang ZX, Wei QY, Chen F (2007) Association between delta-aminolevulinic acid dehydratase (ALAD) polymorphism and blood lead levels: a meta-regression analysis. J Toxicol Environ Health A 70:1986–1994 Flora SJS, Flora G, Saxena G, Mishra M (2007) Arsenic and lead induced free radical generation and their reversibility following chelation. Cell Mol Biol 53:24–46 Gleichmann M, Mattson MP (2011) Neuronal calcium homeostasis and dysregulation. Antioxid Redox Signal 14(7):1261–1273 Hermes-Lima M, Pereira B, Bechara EJH (1991) Are free radicals involved in lead poisoning? Xenobiotica 21:1085–1090 Sandhir R, Julka D, Gill KD (1994) Lipoperoxidative damage on lead exposure in rat brain and its implications on membrane bound enzymes. Pharmacol Toxicol 74:66–71 Schwartz BS, Lee BK, Lee GS (2000) Associations of blood lead, dimercaptosuccinic acid-chelatable lead and tibia lead with polymorphisms in the vitamin D receptor and 5-aminolevulinic acid dehydratase genes. Environ Health Perspect 108:949–954 Shukla PK, Khanna VK, Khan MY, Srimal RC (2003) Protective effect of curcumin against lead neurotoxicity in rat. Hum Exp Toxicol 22(12):653–658 Bolin CM, Basha R, Cox D, Zawia NH, Maloney B, Lahiri DK et al (2006) Exposure to lead and the developmental origin of oxidative DNA damage in the aging brain. FASEB J 20(6):788–790 Blaschke AJ, Weiner JA, Chun J (1998) Programmed cell death is a universal feature of embryonic and postnatal neuroproliferative regions throughout the central nervous system. J Comp Neurol 396:39–50 Antonsson B, Montessuit S, Lauper S, Eskes R, Martinou JC (2000) Bax oligomerization is required for channel-forming activity in liposomes and trigger cytochrome c release from mitochondria. Biochem J 345:271–278 Hengartner MO (2000) The biochemistry of apoptosis. Nature 407:770–776