Effect of Folic Acid and Vitamin-C Administration on Paraoxonase and Arylesterase -1 Activities in Rats intoxicated with Lead
الموضوعات :
Ibrahim Abdulwaliyu
1
,
Stanley Okoduwa
2
,
Shefiat O. Arekemase
3
,
Aliyu Muhammad
4
,
Sani Ibrahim
5
,
Elewechi Onyike
6
1 - Department of Basic Research, National Research Institute for Chemical Technology, Zaria, Nigeria|Department of Biochemistry, Ahmadu Bello University, Zaria, Nigeria
2 - Directorate of Research and Development, Nigerian Institute of Leather and Science Technology, Zaria, Nigeria|Department of Biochemistry, School of Basic Medical Sciences, Babcock University, Ilishan-Remo, Nigeria
3 - Department of Biochemistry, Ahmadu Bello University, Zaria, Nigeria|Petrochemical and Allied Department, National Research Institute for Chemical Technology, Zaria, Nigeria
4 - Department of Biochemistry, Ahmadu Bello University, Zaria, Nigeria
5 - Department of Biochemistry, School of Basic Medical Sciences, Babcock University, Ilishan-Remo, Nigeria
6 - Department of Biochemistry, Ahmadu Bello University, Zaria, Nigeria
تاريخ الإرسال : 12 الخميس , ذو الحجة, 1442
تاريخ التأكيد : 21 الأربعاء , ربيع الأول, 1443
تاريخ الإصدار : 24 الجمعة , صفر, 1443
الکلمات المفتاحية:
vitamin C,
Lead,
Lipid profile,
folic acid,
Paraoxonase/aryl-esterase-1,
PON-1,
ملخص المقالة :
Paraoxonase and aryl-esterase-1 (PON-1) in serum of rats intoxicated with lead then administered Folic acid and Vitamin-C was investigated in forty male albino rats (160-190 g) randomly separated into 2 groups of 20 rats each namely: Lead acetate (60 mg kg -1) and normal saline was given to each group for 6 weeks and there after administered Folic acid (500 µg kg -1) and/or Vitamin-C (60 mg kg-1) orally for 4 weeks. Blood sample was obtained at the end from each rat for biochemical assessment. Results obtained indicated significant (p<0.05) reduction in activities of arylesterase (60.51±8.52 U L-1) and paraoxonase (74.95±3.63 U L-1) of non-supplemented, rats intoxicated with lead compared to 121.51±7.34 and 98.19±2.25 U L-1 respectively for the control groups. Similarly, the values of catalase (10.54±0.46 U mg-1) and superoxide dismutase (4.93±0.66 U mg-1), differ significantly (p<0.05) in the non-supplemented group intoxicated with lead as compared to 31.62±0.67 U mg-1, and 28.46±1.54 U mg-1 respectively for the control groups. Malonyldialdehyde level (0.58±0.29 nmol L-1) decreased significantly (p<0.05) in the control group as compared to the 5.21±0.16 nmol L-1 observed in the non-supplemented group intoxicated with lead. Significant (p<0.05) decrease was observed for high-density lipoprotein cholesterol level (41.08±0.48 mg L-1) in the non-supplemented, rats intoxicated with lead as compared to the level (78.67±0.66 mg L-1) noticed in the control group. Findings from this study deduced that sub-chronically lead intoxication may cause cardiovascular diseases as evident in the decreased activities of arylesterase and paraoxonase. However, administration of Folic acid and Vitamin-C to the rats intoxicated with lead improves the catalytic activities of PON-1, and this may mitigate lead-induced cardiovascular disease risk.
المصادر:
Mahmoudi R., Kazeminia M., Kaboudri A., Pir-Mahalleh S.F., Pakbin B., 2017. A review of the importance, detection and controlling of heavy metal in milk and dairy product. Malaysian Journal of Science. 36(1), 1-16.
Golalipour M.J., Roshandel D., Roshandel G., Ghafari S., Kalavi M., Kalavi K., 2007. Effect of Lead Intoxication and D-penicillamine Treatment on Haematological Indices in Rats. Int J Morphol. 24(4),717-22.
Ramah A., El-shwarby R.M., Nabila M.A., El-shewey E.A., 2015. The Effect of Lead Toxicity on Male Albino Rats Reproduction Ameliorated by Vitamin E and Pumpkin Seed Oil. Benha Vet Med J. 28(1), 43-52.
Candido G.S., Martins G.C., Vasques I.C.F., Lima F.R.D., Pereira P., Engelhardt M.M., Reis R.H.C.L., Marques J.J., 2020. Toxic effects of lead in plants grown in Brazilian soils. Ecotoxicity. 29(3), 305-313. doi: 10. 1007/s10646-020-02174-8.
Shiek S.S., Mani M.S., Kabekkodu S.P., Dsouza H.S., 2021. Health repercussions of environmental exposure to lead: methylation perspective. Toxicology. 461, 152927. Doi.org/10.1016/j.tox.2021.152927.
Adhikari N., Sinha N., Narayan R., 2001. Lead-Induced Cell Death in Testes of Young Rats. J App Toxicol. 21, 275-27.
Nemsadez T., Sanikidze L., Ratiani L., Gabunia T., Sharashenidze T., 2009. Mechanism of Lead-Induced poisoning. Georgian. Med News. 172-3, 92-6.
Game E.M., Dasilva L.A., Lemos V.A., 2006. Preconcentration System for Cadmium and Lead Determination in environmental Samples Using Polyurethane foam/ Me-BTANC. J Hazard Mat. 36, 757-62.
Ebuehi Q.A.T., Ogedebge R.A., Ebuehi O.M., 2012. Oral Administration of Vitamin C and Vitamin E Ameliorate Lead Hepatotoxicity and Oxidative Stress in the Rat Brain. Nig Qt J Hosp Med. 22(2), 85-90.
Ekanem A.U., Kwari H.D., Garba S.H., Salami H.A., 2015. Effect of Lead Acetate on Spleen and Blood Parameters in Albino Rats. J Dental Med Sci. 14(3),43-9.
Lysenco M., 2005. Unithiol-The means of Preventing Lead Accumulation in Tissues and Organs of Broilers. Conference Information: Proceedings of the XVII European Symposium on the Quality of the Poultry meat and European Symposium on the Quality of Eggs Products. Golden Tulip ParkhotelDooowert, Doowerth, Netherland, 23-6.
Utemba W., Gulumian M., 2021. Issues and challenges in the application of the IEUBK model in the health risk assessment of lead: a case study from Blantyre Malawi. International Journal Environmental Research and Public Health. 18, 8207. Doi.org/10.3390/ijerph 18158207.
Mahmoudi R., Mardani K., Rahimi B., 2015. Analysis of heavy metals in honey from North-Western regions of Iran. Journal of Chemical Health Risk. 5(4), 251-6.
Seven I., Aksu T., Seven P.T., 2010. The Effect of Proposlis on Biochemical Parameters and Activity of Antioxidants Enzymes in Briolers Exposed to Lead-Induced Oxidative Stress. Asian -Australian J Ani Sci. 23(11), 1482-9.
Dister S., Saikawa E., 2020. A new screening index to better target low level lead exposure in Atlanta, Geogia Sci Rep. 10, 18087. Doi.org/10.1038/s41598-020-75000-0.
Chowdhury K.I.A., Nurunnahar S., Kabir M.L., Islam M.T., Baker M., Islam S.M., Rahman M., Hassan M., Sikder A., Kwong L.H., Binkhorst G.K., Nash E., Keith J., McCarton A., Luby S.P., Forysth J.E., 2021. Child lead exposure near abandoned lead acid battery recycling sites in a residential community in Bangladesh: risk factors and the impact of soil remediation on blood lead levels. Environmental Research. 194, 110689.
Flora G., Gupta D., Tiwari A., 2012. Toxicity of Lead: A review with recent updates. Interdisci Toxicol. 5(2),47-58.
Claveland L.M., Minter M.L., Cobbs K.a., Scott A.A., German V.F., 2008. Lead hazards for pregnant women and childern. Part 1: American J Nutri. 108,40-9.
Hernandez A.F., Gil F., Leno E., Lopez O., Rodrigo L., Pla A., 2009. Interaction between human serum esterases and environmental metal compounds. Neurotoxicol. 30, 628-5.
Huen K., Richter R., Furlong C., Eskenazi B., Holland N., 2009. Validation of Pon1 enzyme activity assays for longitudinal studies. Clin Chem Acta. 402, 67-74.
Li W.F., Pan M.H., Chung M.C., Ho C.K., Chuang H.Y., 2006. Lead Exposure is Associated with Decrease Serum Paraoxonase 1 (PON1) Activity. J Env Health Perspect. 114(8), 1233-6.
Lamas G.A., Ujueta F., Navas-Acien A., 2021. Lead and cadmium as cardiovascular disease risk factors. The burden of proof has been met. Journal of the American Hearth Association, 10.e018692. doi: 10.1161/JAHA.120.018692.
Quan F.S., Yu, X.F. and Ren, W.Z. 2015. Protective Effects of Folic acid against Central Nervous System Neurotoxicity Induced by Lead Exposure in rats Pups. Gen Mol Res. 14(4),12467-71.
Tveden-Nyborg P., Bergmann T.K., Jessen N., Simonsen U., Lykkesfeldt J., 2021. BCPT policy for experimental and clinical studies. Basic Clin. Pharmacol. Toxicol. 128, 4-8.
Eckerson H.W., Wyte C.M., Ladu B.N. 1983. The human Serum paraoxonase/aryl-esterase polymorphism. Am J Hum Genet, 35,1126-38.
Mogarekar M.R., Chawhan S.S., 2013. The determination of Q192R polymorphism of paraoxonase 1 by using nontoxic substrate p-nitrophenyl-acetate. Ind J Hum Genet. 19(1),71-7.
Placer Z.A., Linda L., Crushman J.B.C., 1996. Estimation of product of lipid peroxidation in biochemical system. Annal Biochem. 16, 359 – 64.
Prakask B.D., Manjunath S., Sunmangala K., Chatana K., Vanishree J., 2010. Oxidative stress and enzymatic antioxidant status in rheumatoid arthritis: A case control study. Eur Rev Med Pharmacol Sci. 14, 959-67.
Aebi H., Catalase invitro. Methods in ezymology. ClockwickSp, Kaplan editors. Acad. Press. 105,114-21.
Fridovich I., 1989. Superoxide dismutase. An adaptation to a paramagnetic gas. J Biol Chem. 264, 7761-4.
Permpongpaiboon T., Nagila A., Pidetha P., Tuangmungsakulchai K., Tantrarongroi S., Portadavity S., 2011. Decreased Paraoxonase 1 Activity and Increased Oxidative stress in low Lead Exposed Workers. J Hum Exp Toxic. 30(9),1196-203.
Gursu F.M., Onderci M., Kazim, S., 2004. Effects of Vitamin C and Folic acid Supplementation on Serum Paraoxonase activity and Metabolite Induced by Heat stress in vivo. Nutri. Res. 24(2),157-64.
Kamal M., Fathy M.M., Taher E., Hassan M., Tolba M., 2011. Assessment of the Role of Paraoxonase gene Polymorphism (Q192R) and Paraoxonase Activity in the Susceptibility to Artherosclerosis among Lead Exposed Workers. Ann Saudi Med. 3(15), 481-7.
Jarvic G.P., Tsai N.T., Mckinstry L.A., Wani R., Brophy V.H., Richter R.J., Schellenberg G.D., Heagetry P.J., Hatsukami T.S., Furlong C.E., 2002. Vitamin C and E intake is associated with paraoxonase activity. J Arterio Thromb Vas Bio. 22,1329-33.
Dashty M., Motazacker M.M., Levels J., Devaris M., Mahmoudi M., Peppelenbosch M.P., Rezaee F., 2014. Proteome of Human Plasma, very low-density lipoprotein and low-density lipoprotein Exhibits a link with Coagulation and Lipid Metabolism. J Thromb Haemost. 23 (111), 518-530.
Sa’ad R.A., El-Sayed M.H., 2014. Hemodynamic and Cardiac Function in Rats Exposed to Lead Toxicity: The Possible Effects of Vitamin C. J Life Sci. 11(7), 167-79.
Gajawat S., Sancheti G., Goyal P.K., 2006. Protection against Lead-Induced Hepatic Lesions in Swiss albino mice. J Pharmacol line. 1,140-9.
Kojima M., Masur T., Wemoto K., Degawa M., 2004. Lead nitrate induced development of hypercholesterolemia in rats: Sterol independent gene regulation of hepatic enzyme responsible for cholesterol homeostasis. Toxicol Lett. 1547, 35-44.
Mohammadin Z., Eidi A., Mortazavi P., Tavangar S.M., Aschari A., 2015. Effects of Folic acid on Dyslipidemia and Serum Homocysteine in a rat Model of Cholestasis and Hepatic Fibrosis. J Pathol. 66(1),49-56.
Woo C.W., Siow Y.L., Pierce G.N., 2005. Hyperhomocysteinemia Induces Hepatic Cholesterol Biosynthesis and Lipid Accumulation via Activation of Transcription Factor. Am J Physiol End Met. 288,102-10.
Mecif O.K., Bouguerra S.A., Benazzoug Y., 2017. Plasma and Aorta Biochemistry and MMPs Activities in Female Rabbit Fed Methionine Enriched Diet and their Offspring. J Nut Meth. http://doi.org/10.1155/2785142.
Samouilidou E., Kostopoulous V., Liaouri A., Kioussi E., Vassiliou K., Bountou E., Grapsa E., 2016. Association of lipid profile with serum pon1 concentration in patients with chronic kidney disease. J Ren Fail. 38(10),1601-7.
Sharma S., Sharma V., Paliwal R., 2011. Lead Toxicity Oxidative damage and Health Implication: A Review. Int J Biotech Mol Bio Res. 2(13), 215-21.
Seven T.P., Seven I., Yilmaz M., Simek G., 2008. The Effect of Turkish Propils on Growth and Carcass Characteristics in Broilers under heat stress. Ani Fd Sci Tech.146, 137-48.
Wang C., Liang J., Zhang C., Bi Y., Shi X.M., Shi Q., 2007. Effect of Ascorbic acid and Thiamin Supplementation at Different Concentration on Lead Toxicity in Rats. Ann Occup Hyg. 51(6),563-9.
Ramana V.Ch., 2014. Study of serum malondialdehyde, paraoxonase and lipid profile in pregnancy with preeclampsia and normal pregnancy. J Pharm Bio Sci. 9(3), 13-18.
Patil P.V., Pahil A.B., Patil V.S., Ingleshwar D.G., 2016. Paraoxonase activity and lipid profile in paediatic Nephrotic syndrome; A cross sectional study. J Clin Diag Res. 10(3), 17-20.
Cheng W.L., Zhang Q., Cao J.L., Chen X.L., Li W., Zhang L., Chao S.P., Zhao F., 2021. ALK7 acts as a positive regulator of macrophage activation through down-regulation of PPARγ expression. Journal of Atherosclerosis and Thrombosis. 28(4), 375-84.
