Author(s): KM Diksha Singh, Vikram Singh, Adity Singh, Vipin Kesharwani

Email(s): diks83282@gmail.com

DOI: 10.52711/0974-360X.2021.01072   

Address: KM Diksha Singh1*,Vikram Singh2, Adity Singh1, Vipin Kesharwani1
1Department of Pharmacology, Student of Shambhunath İnstitute of Pharmacy, Jhalwa, Prayagraj, Uttar Pradesh - 211012, India.
2Department of Pharmacology, Faculty of Shambhunath Institute of Pharmacy, Jhalwa, Prayagraj, Uttar Pradesh - 211012, India.
*Corresponding Author

Published In:   Volume - 14,      Issue - 12,     Year - 2021


ABSTRACT:
Background: Oxidative stress is imbalance between aggressive and defensive system. Overproduction of oxidative stress contribute in pathogenesis of many diseasesincluding Parkinsonism, Alzheimer diseases, apoptosis, hepatic fibrosis ,chronic kidney failure and liver steatosis etc . There are several OTC drugs including NSAIDs that generate oxidative stress when administered. So there is a need to explore about these drugs. Therefore this study was designed to evaluate the oxidative stress potential of Acetaminophen, acetyl salicylic acid and Celecoxib NSAIDs. Objective: The present study is design to investigate the oxidative stress of NSAIDs of acetaminophen, aspirin and Celecoxib drug with reference to the hydrogen peroxide. Material and method: The Experimental protocol was designed for estimate the level of oxidative stress in NSAIDs treated animals against hydrogen peroxides. Animal of control group received only vehicle throughout experimental protocol. Rats of AAP group, ASA group ,CX group were exposed to acetaminophen (150mg/kg; orally) acetyl salicylic acid (300mg/kg ;orally) and Celecoxib (50mg/kg; orally) for forty two days . Rodent of HP group were challenged with Hydrogen peroxides (0.5%) with same schedule as above. At end of experimental protocols, all the animals were sacrificed and their organ were identified and collected for oxidative stress estimation and histological examination. Result: NSAIDs administration caused increase in oxidative stress measured in terms of SOD, CAT, MDA, GSH and GPx. HP administration produced maximum oxidative stress compare to all other groups. Oxidative parameter i.e. SOD, CAT, GSH and GPx were found to be decreased as compare to control rats. However MDA were found to be increased as compare to control rats. Additionally, CX produced less oxidative stress compare to other NDAIDs. Further, histological examinations support the biochemical results. Conclusion: From the above observations it can be concluded that NSAIDs have oxidative stress potential and generate oxidative stress and damage the organs when administrated chronically. Thus, these drugs should be used judiciously.


Cite this article:
KM Diksha Singh,Vikram Singh, Adity Singh, Vipin Kesharwani. Evaluation of Oxidative Stress potential of some Nsaıds against Hydrogen Peroxide in experimental animal. Research Journal of Pharmacy and Technology. 2021; 14(12):6194-0. doi: 10.52711/0974-360X.2021.01072

Cite(Electronic):
KM Diksha Singh,Vikram Singh, Adity Singh, Vipin Kesharwani. Evaluation of Oxidative Stress potential of some Nsaıds against Hydrogen Peroxide in experimental animal. Research Journal of Pharmacy and Technology. 2021; 14(12):6194-0. doi: 10.52711/0974-360X.2021.01072   Available on: https://www.rjptonline.org/AbstractView.aspx?PID=2021-14-12-2


REFERENCE:
1.    Gutteridge IBH. Antioxidants in Nutrition, Health and Disease. Oxford, Oxford University Press.; 1994,
2.    Powers SK, Ji LL, Kavazis AN, Jackson MJ. 2011. Reactive Oxygen Species: Impact on Skeletal Muscle. Compr Physiol. 2(1): 941–69.
3.    Cho C-H, Lee H-J. Oxidative Stress and Tardive Dyskinesia: Pharmacogenetic Evidence. Progress in Neuro Psychopharmacology and Biological Psychiatry. 2013; 13:207.
4.    Hofer T, Perry G. Nucleic Acid Oxidative Damage in Alzheimer’s Disease-Explained by the Hepcidin-Ferroportin Neuronal Iron Overload Hypothesis? Journal of Trace Elements in Medicine and Biology: Organ of the Society for Minerals and Trace Elements GMS. 2016
5.    Nelson SD. Molecular Mechanisms of the Hepatotoxicity Caused by Acetaminophen. Semin Liver. 1990; 90: 267–78.
6.    Jollow DJ, Mitchell JR, Potter WZ, Davis DC, Gillette, and Brodie BB. JR. Acetaminophen-Induced Hepatic Necrosis. II. Role of Covalent Binding in Vivo. J Pharmacol Exp Ther. 1973,187: 195–202.
7.    Ajith TA, Hema U, Aswathy MS.  Zingiber officinale Roscoe Prevents Acetaminophen-Induced Acute Hepatotoxicity by Enhancing Hepatic Antioxidant Status. Food Chem Toxicol. 2007; 45(11): 2267–72.
8.    McCarthy DM. Mechanism of Mucosal Injury and Healing: The Role of Non-Steroidal Anti-Inflammatory Drugs. J Gastroenterol. 1995; 208: 24–29.
9.    Fossline E. Adverse Effects of Non-Steroidal Anti Inflammatory Drugs on the Gastrointestinal System. Ann Clin Lab Sci. 1998; 28: 67–81.
10.    Article.  L Ipid Peroxidation and Oxidative Stress in Rat Erythrocytes Induced by Aspirin and Diazinon : The Protective Role of Selenium. 2014; 4(Suppl 2).
11.    Engelhart MJ, Geerlings MI, A. Ruitenberg et al. Dietary Intake of Antioxidants and Risk of Alzheimer Disease. JAMA. 2002; 287(24): 3223–29.
12.    De Belleroche, J., Orrell, R. and King, A.  Familial Amyotrophic Lateral Sclerosis/Motor Neuron Disease (FALS): A Review of Current Developments. Journal of Medical Genetics. 1991; 32: 841–47. Engelhart MJ, GeerlingsMI, A. Ruitenberg et al. Dietary Intake of Antioxidants and Risk of Alzheimer Disease. JAMA. 2002; 287(24): 3223–29.
13.    Bamford, K.A., Caine, E.D., Kido, D.K., Cox, C. and Shoulson, I. A Prospective Evaluation of Cognitive Decline in Early Huntington’s Disease: Functional and Radiographic Correlates. Neurology. 1995; 45: 1867–73.
14.    Pizzino G, Irrera N, Cucinotta M, et al. Oxidative Stress: Harms and Benefits for Human Health. Oxidative Medicine and Cellular Longevity,  2017(Article ID 8416763,): 13.
15.    Aravinthan AD, Alexander GJ. Senescence in Chronic Liver Disease: Is the Future in Aging. Journal of Hepatology. 2016; 65: 825–34.
16.    Fatma, Guesmi, Bellamine Houda, and Landoulsi Ahmed. H2O2-Induced Oxidative Stress , AChE Inhibition and Mediated Brain Injury Attenuated by Thymus Algeriensis. Applied Physiology, Nutrition and Metabolism . 1–23.
17.    Dayal S, Baumbach GL, Arning E, Bottiglieri T, Faraci FM, Lentz SR.  Deficiency of Superoxide Dismutase Promotes Cerebral Vascular Hypertrophy and Vascular Dysfunction in Hyperhomocysteinemia. PloS One.  2017; 12: 175732.
18.    Gill SS, Tuteja N. Reactive Oxygen Species and Antioxidant Machinery in Abiotic Stress Tolerance in Crop Plants. 2010.  909–30.
19.    Góth L, Rass P, Páy A. Catalase Enzyme Mutations and Their Association with Diseases.  2004 : 141–49.
20.    Gutteridge IBH. Antioxidants in Nutrition, Health and Disease. Oxford, Oxford University Press. 1994,
21.    Chabory E, Damon C, Lenoir A, et al. Epididymis Seleno-Independent Glutathione Peroxidase 5 Maintains Sperm DNA Integrity in Mice. J Clin Invest. 2009; 119: 2074.
22.    Asaduzzaman Khan M, Tania M, Zhang DZ, Chen HC.  Antioxidant Enzymes and Cancer. 2010, 87–92.
23.    Vignesh Balaji. E, Tamil Selvan. A, Srinivasan. A, Nandhini. S. Punica granatum root (s): Phytocompounds analysis, Anti-oxidant and Anti-microbial activity. Asian J. Pharm. Ana. 2019; 9(3):123-127.

Recomonded Articles:

Research Journal of Pharmacy and Technology (RJPT) is an international, peer-reviewed, multidisciplinary journal.... Read more >>>

RNI: CHHENG00387/33/1/2008-TC                     
DOI: 10.5958/0974-360X 

0.38
2018CiteScore
 
56th percentile
Powered by  Scopus


SCImago Journal & Country Rank


Recent Articles




Tags


Not Available