تاثیر دو ماه تمرین تناوبی شدید همراه با مکمل سیترات سدیم بر وضعیت ردوکس درون سلولی و شاخص های فشار اکسایشی در رت های نردیابتی

نوع مقاله : مقاله پژوهشی Released under (CC BY-NC 4.0) license I Open Access I

نویسندگان

گروه فیزیولوژی ورزشی، دانشکده علوم تربیتی و روانشناسی، دانشگاه محقق اردبیلی، اردبیل، ایران

چکیده

هدف: تغییر سیگنال ردوکس سلولی در بروز دیابت و توسعه عوارض آن، موثر می‌باشد، لذا هدف از پژوهش حاضر بررسی تاثیر دو ماه تمرین تناوبی شدید همراه با مصرف مکمل سیترات سدیم بر وضعیت ردوکس درون سلولی و شاخص های فشار اکسایشی در قلب رت‌های نردیابتی بود. روش پژوهش: این پژوهش مداخله‌ای با 50رت صحرایی نر سفید سه‌ماهه با دامنه وزنی (225 الی 300 گرم) در پنج گروه کنترل سالم، کنترل دیابتی، دیابتی - تمرین، دیابتی- مکمل دهی سیترات سدیم و دیابتی-مکمل دهی سیترات سدیم-تمرین (10=N) تقسیم شدند. رت‌های دو گروه تمرین و تمرین+ مکمل به مدت 8 هفته و 5 روز در هفته تمرینات تناوبی را با شدت 90 درصد حداکثر سرعت دویدن بر روی تردمیل اجرا کردند. رت‌های گروه تمرین+ مکمل علاوه بر اجرای تمرین، روزانه 15 میلی‌مول/ لیتر از مکمل سیترات سدیم را به‌صورت محلول در آب دریافت کردند. شاخص‌های فشاراکسایشی با استفاده از کیت­ الایزا شرکت BioSource محصول آمریکا با میزان ضرایب تغییرات 15% اندازه گیری شد. تجزیه تحلیل داده‌ها با استفاده از آزمون آماری آنالیز واریانس یک‌طرفه و آزمون تعقیبی LSD در نرم افزار26SPSS انجام شد (05/0≥p). یافته‌ها: سطح (GSH، GSSG، GSH/GSSG و SOD) دربین گروه سالم و دیابتی اختلاف معنی­داری داشت (05/0≥p). تمرین تناوبی شدید و مصرف مکمل سیترات سدیم موجب افزایش معنادار سطح (GSH، GSH/GSSG و SOD) در گروه دیابتی- مکمل و دیابتی- مکمل- تمرین شد که با توجه به اختلاف میانگین­ها، این افزایش در گروه دیابتی-مکمل بیشتر بوده است. کاهش معنی­داری در سطح GSSG در گروه دیابتی-مکمل و دیابتی-مکمل-تمرین در مقایسه با گروه دیابتی - تمرین وکنترل-دیابتی مشاهده شد (05/0≥p) و اختلاف میانگین­ها نشان داد این کاهش سطح GSSG در گروه دیابتی- مکمل- تمرین نسبت به سایر گروه های دیابتی بیشتر بوده است. نتیجه‌گیری: نتایج مطالعه حاضر نشان داد که تمرین تناوبی با شدت 90 درصد حداکثر سرعت دویدن می‌تواند شاخص های استرس اکسیداتیو را در قلب موش های صحرایی دیابتی افزایش دهد لذا توصیه می شود این نوع ورزش با احتیاط و با استفاده از مکمل سیترات سدیم یا سایر مکمل های آنتی اکسیدانی در بیماران دیابتی انجام شود.

کلیدواژه‌ها

موضوعات

عنوان مقاله [English]

The effect of two months of intense intermittent exercise with sodium citrate supplementation on intracellular redox status and oxidative stress indices in diabetic rats

نویسندگان [English]

  • Malahat Kashfi Moghadam
  • Farnaz Seyffi Eskishahr
  • Roghayyeh Afroundeh
  • Lotfali Bolboli
Department of Sport Physiology, Faculty of Educational Sciences and Psychology, University of Mohaghegh Ardabili, Ardabil, Iran
چکیده [English]

Aim:      Alteration of cellular redox signal is effective in the incidence of diabetes and the development of its complications, so the aim of this study was to investigate the effect of two months high-intensity interval training with sodium citrate supplementation on intracellular redox status and oxidative stress indices in the heart of diabetic rats. Methods: This interventional study was performed on 50 white male rats (3 months old) with weight rang of 225-300 g in five groups: healthy control, diabetic control, diabetic-training, diabetic-sodium citrate supplementation, and diabetic-sodium citrate supplementation-training. Rats in both groups of training and training + supplementation performed interval training with an intensity of 90% of maximum running speed on a treadmill for 8 weeks, 5 days a week. In addition to the exercise, the rats in the exercise+supplement group received 15 mmol/L of sodium citrate supplement in the form of water soluble daily. Oxidative stress indices were measured using the ELISA kit with a coefficient of variation of 15%. Data were analyzed using one-way ANOVA and LSD post hoc test in SPPS26 statistical software (p<0.05). Results:  There was a significant difference between the healthy and diabetic groups in the levels of GSH, GSSG، GSH/GSSG, SOD (p<0.05). The level of GSH, GSH/GSSG, and SOD were lower in high-intensity interval training compared to diabetic control group (p<0.05) but sodium citrate supplementation significantly increased the level of these variables in diabetic rats. Significant reduction in the level of GSSG was observed in the diabetic-supplement and diabetic-supplement-exercise groups, compared to the diabetic-exercise and control-diabetic groups (p<0.05). The difference in the means showed that this decrease in GSSG level was more in the diabetic-supplement-exercise group compared to the other diabetic groups.
Conclusions The results of the present study showed that interval training with an intensity of 90% of the maximum running speed can increase oxidative stress indices in the heart of diabetic rats, so it is recommended to do this type of exercise with caution and using sodium citrate supplementation or other antioxidant supplements in diabetic patients.

کلیدواژه‌ها [English]

  • Sodium citrate
  • intracellular redox
  • oxidative stress indicators
  • diabetes

مراجع

  1. Carracher AM, Marathe PH, Close KL. International diabetes federation 2017. Wiley Online Library; 2018.
  2. Burgos-Morón E, Abad-Jiménez Z, Martínez de Marañón A, Iannantuoni F, Escribano-López I, López-Domènech S, et al. Relationship between oxidative stress, ER stress, and inflammation in type 2 diabetes: the battle continues. Journal of clinical medicine. 2019;8 (9):1385.
  3. Zhang P, Li T, Wu X, Nice EC, Huang C, Zhang Y. Oxidative stress and diabetes: antioxidative strategies. Frontiers of medicine. 2020;14:583-600.
  4. Das KC, White CW. Redox systems of the cell: possible links and implications. Proceedings of the National Academy of Sciences. 2002;99 (15):9617-8.
  5. Le Gal K, Schmidt EE, Sayin VI. Cellular redox homeostasis. Antioxidants. 2021;10 (9):1377.
  6. Folli F, Corradi D, Fanti P, Davalli A, Paez A, Giaccari A, et al. The role of oxidative stress in the pathogenesis of type 2 diabetes mellitus micro-and macrovascular complications: avenues for a mechanistic-based therapeutic approach. Current diabetes reviews. 2011;7 (5):313-24.
  7. Asmat U, Abad K, Ismail K. Diabetes mellitus and oxidative stress—A concise review. Saudi pharmaceutical journal. 2016;24 (5):547-53.
  8. Sosa V, Moliné T, Somoza R, Paciucci R, Kondoh H, LLeonart ME. Oxidative stress and cancer: an overview. Ageing research reviews. 2013;12 (1):376-90.
  9. Giancarlo A. Biomarkers for antioxidant defense and oxidative damage: principles and practical applications/Giancarlo Aldini: Wiley-Blackwell; 2010.
  10. El-Hefny MA, Karimova ST, Afandiev AM. Lipid peroxidation and antioxidant status in breast cancer patients before and after therapy. Med J Cairo Univ. 2009;77:37-42.
  11. Salmaninejad A, Kangari P, Shakoori A. Oxidative stress: development and progression of breast cancer. Tehran University Medical Journal TUMS Publications. 2017;75 (1):1-9.
  12. Steinbacher P, Eckl P. Impact of oxidative stress on exercising skeletal muscle. Biomolecules. 2015;5 (2):356-77.
  13. Mohammadi E, Nikseresht F. Effect of 8 weeks of incremental endurance training on the activity of superoxide dismutase enzyme and malondialdehyde levels of cardiac tissue of rats with type 2 diabetes. Iranian Journal of Diabetes and Metabolism. 2020;19 (5):261-8.
  14. Seifi-Skishahr F, Damirchi A, Farjaminezhad M, Babaei P. The Comparison of One-Session Intensive Aerobic Exercise Effects on Glutathione Redox State of Red Blood Cells in Professional, Recreational Athletes and Nonathletes. Journal of Ardabil University of Medical Sciences. 2015;15 (1):25-38.
  15. Naderi R, Mohaddes G, Mohammadi M, Ghaznavi R, Ghyasi R, Vatankhah AM. Voluntary exercise protects heart from oxidative stress in diabetic rats. Advanced pharmaceutical bulletin. 2015;5 (2):231.
  16. Moldoveanu B, Otmishi P, Jani P, Walker J, Sarmiento X, Guardiola J, et al. Inflammatory mechanisms in the lung. Journal of inflammation research. 2008:1-11.
  17. Ganjifrockwala FA, Joseph J, George G. Decreased total antioxidant levels and increased oxidative stress in South African type 2 diabetes mellitus patients. Journal of Endocrinology, Metabolism and Diabetes of South Africa. 2017;22 (2):21-5.
  18. van der Schaft N, Schoufour JD, Nano J, Kiefte-de Jong JC, Muka T, Sijbrands EJ, et al. Dietary antioxidant capacity and risk of type 2 diabetes mellitus, prediabetes and insulin resistance: the Rotterdam Study. European journal of epidemiology. 2019;34:853-61.
  19. Burke L, Cort M, Cox G, Crawford R, Desbrow B, Farthing L, et al. Supplements and sports foods. Clinical sports nutrition. 2006;3:485-580.
  20. Carr AJ, Hopkins WG, Gore CJ. Effects of acute alkalosis and acidosis on performance: a meta-analysis. Sports medicine. 2011;41:801-14.
  21. Urwin CS, Snow RJ, Condo D, Snipe R, Wadley GD, Carr AJ. Factors influencing blood alkalosis and other physiological responses, gastrointestinal symptoms, and exercise performance following sodium citrate supplementation: a review. International journal of sport nutrition and exercise metabolism. 2021;31 (2):168-86.
  22. Thomas C, Bishop D, Moore-Morris T, Mercier J. Effects of high-intensity training on MCT1, MCT4, and NBC expressions in rat skeletal muscles: influence of chronic metabolic alkalosis. American Journal of Physiology-Endocrinology and Metabolism. 2007;293 (4):E916-E22.
  23. Katz A, Costill D, King D, Hargreaves M, Fink W. Maximal exercise tolerance after induced alkalosis. International journal of sports medicine. 1984;5 (02):107-10.
  24. Xia T, Yang Y, Li W, Tang Z, Huang Q, Li Z, et al. Meditative movements for patients with type 2 diabetes: a systematic review and meta-analysis. Evidence-Based Complementary and Alternative Medicine. 2020;2020.
  25. Gao L, Wang W, Liu D, Zucker IH. Exercise training normalizes sympathetic outflow by central antioxidant mechanisms in rabbits with pacing-induced chronic heart failure. Circulation. 2007;115 (24):3095-102.
  26. Tang Z, Wang Y, Zhu X, Ni X, Lu J. Exercise increases cystathionine-γ-lyase expression and

decreases the status of oxidative stress in myocardium of ovariectomized rats. International heart journal.

2016;57 (1):96-103.

  1. Farhangi N, Nazem F, Zehsaz F. Effect of endurance exercise on antioxidant enzyme activities

and lipid peroxidation in the heart of the streptozotocin-induced diabetic rats. SSU_Journals.

2017;24 (10):798-809.

  1. Simioni C, Zauli G, Martelli AM, Vitale M, Sacchetti G, Gonelli A, et al. Oxidative stress: role of physical exercise and antioxidant nutraceuticals in adulthood and aging. Oncotarget. 2018;9 (24):17181.
  2. Rezaee S, Barari A, Ahmadi M. Effect of eight weeks aerobic training on the levels of antioxidant enzymes in the heart tissue of type 2 diabetic rats. 2020.
  3. Abdi A, Ramezani N, Abbasi Daloie A, Ganji N. The effect of aerobic training and Coriandrum sativum extract on some oxidative stress factors in male diabetic Wistar rats. Tabari Biomedical Student Research Journal. 2017;2 (4):34-43.
  4. Kanter M, Aksu F, Takir M, Kostek O, Kanter B, Oymagil A. Effects of low intensity exercise against apoptosis and oxidative stress in Streptozotocin-induced diabetic rat heart. Experimental and Clinical Endocrinology & Diabetes. 2017;125 (09):583-91.
  5. Vincent AM, Russell JW, Low P, Feldman EL. Oxidative stress in the pathogenesis of diabetic neuropathy. Endocrine reviews. 2004;25 (4):612-28.
  6. Manna I, Jana K, Samanta PK. Intensive swimming exercise-induced oxidative stress and reproductive dysfunction in male Wistar rats: protective role of α-tocopherol succinate. Canadian Journal of Applied Physiology. 2004;29 (2):172-85.
  7. Thirumalai T, Therasa SV, Elumalai E, David E. Intense and exhaustive exercise induce oxidative stress in skeletal muscle. Asian Pacific Journal of Tropical Disease. 2011;1 (1):63-6.
  8. Covas M-I, Elosua R, Fitó M, Alcántara M, Coca L, Marrugat J. Relationship between physical activity and oxidative stress biomarkers in women. Medicine & Science in Sports & Exercise. 2002;34 (5):814-9.
  9. Ramel A, Wagner K-H, Elmadfa I. Plasma antioxidants and lipid oxidation after submaximal resistance exercise in men. European journal of nutrition. 2004;43:2-6.
  10. Stocker R, Keaney Jr JF. Role of oxidative modifications in atherosclerosis. Physiological reviews. 2004;84 (4):1381-478.
  11. Cantin AM. Potential for antioxidant therapy of cystic fibrosis. Current opinion in pulmonary medicine. 2004;10 (6):531-6.
  12. Bonnefont-Rousselot D. The role of antioxidant micronutrients in the prevention of diabetic complications. Treatments in endocrinology. 2004;3:41-52.

40        Viña J, Lloret A, Ortı R, Alonso D. Molecular bases of the treatment of Alzheimer's disease with antioxidants: prevention of oxidative stress. Molecular aspects of medicine. 2004;25 (1-2):117-23.

  1. Berger MM. Can oxidative damage be treated nutritionally? Clinical nutrition. 2005;24 (2):172-83.
  2. Abbas M, Monireh M. The role of reactive oxygen species in immunopathogenesis of rheumatoid arthritis. Iranian Journal of Allergy, Asthma and Immunology. 2008:195-202.
  3. Cutler RG. Genetic stability, dysdifferentiation, and longevity determinant genes. Critical Reviews of Oxidative Stress and Aging: Advances in Basic Science, Diagnostics and Intervention (In 2 Volumes). 2003:1146-235.
  4. Camire ME, Kantor MA. Dietary supplements: nutritional and legal considerations. Food technology (Chicago). 1999;53 (7):87-96.
  5. Myung S-K, Kim Y, Ju W, Choi H, Bae W. Effects of antioxidant supplements on cancer prevention: meta-analysis of randomized controlled trials. Annals of Oncology. 2010;21 (1):166-79.
  6. Lee I-M, Cook NR, Gaziano JM, Gordon D, Ridker PM, Manson JE, et al. Vitamin E in the primary prevention of cardiovascular disease and cancer: the Women’s Health Study: a randomized controlled trial. Jama. 2005;294 (1):56-65.
  7. Hu P, Tirelli N. Scavenging ROS: superoxide dismutase/catalase mimetics by the use of an oxidation-sensitive nanocarrier/enzyme conjugate. Bioconjugate chemistry. 2012;23 (3):438-49.
  8. Spizzirri UG, Iemma F, Puoci F, Cirillo G, Curcio M, Parisi OI, et al. Synthesis of antioxidant polymers by grafting of gallic acid and catechin on gelatin. Biomacromolecules. 2009;10 (7):1923-30.
  9. Hood E, Simone E, Wattamwar P, Dziubla T, Muzykantov V. Nanocarriers for vascular delivery of antioxidants. Nanomedicine. 2011;6 (7):1257-72.
  10. Papadopoulos S, Jürgens KD, Gros G. Protein diffusion in living skeletal muscle fibers: dependence on protein size, fiber type, and contraction. Biophysical journal. 2000;79 (4):2084-94.
  11. Wieghaus KA, Capitosti SM, Anderson CR, Price RJ, Blackman BR, Brown ML, et al. Small molecule inducers of angiogenesis for tissue engineering. Tissue engineering. 2006;12 (7):1903-13.
  12. Forman HJ, Fukuto JM, Torres M. Redox signaling: thiol chemistry defines which reactive oxygen and nitrogen species can act as second messengers. American Journal of Physiology-Cell Physiology. 2004;287 (2):C246-C56.
  13. Choi E-Y, Kim H-J, Han J-S. Anti-inflammatory effects of calcium citrate in RAW 264.7 cells via suppression of NF-κB activation. Environmental toxicology and pharmacology. 2015;39 (1):27-34.
  14. Tiranathanagul K, Jearnsujitwimol O, Susantitaphong P, Kijkriengkraikul N, Leelahavanichkul A, Srisawat N, et al. Regional citrate anticoagulation reduces polymorphonuclear cell degranulation in critically ill patients treated with continuous venovenous hemofiltration. Therapeutic Apheresis and Dialysis. 2011;15 (6):556-64.
  15. Gritters M, Grooteman MP, Schoorl M, Schoorl M, Bartels PC, Scheffer PG, et al. Citrate anticoagulation abolishes degranulation of polymorphonuclear cells and platelets and reduces oxidative stress during haemodialysis. Nephrology Dialysis Transplantation. 2006;21 (1):153-9.
  16. Bryland A, Wieslander A, Carlsson O, Hellmark T, Godaly G. Citrate treatment reduces endothelial death and inflammation under hyperglycaemic conditions. Diabetes and Vascular Disease Research. 2012;9 (1):42-51.
  17. Wu X, Dai H, Liu L, Xu C, Yin Y, Yi J, et al. Citrate reduced oxidative damage in stem cells by regulating cellular redox signaling pathways and represent a potential treatment for oxidative stress-induced diseases. Redox biology. 2019;21:101057.
  18. Bishop D, Edge J, Davis C, Goodman C. Induced metabolic alkalosis affects muscle metabolism and repeated-sprint ability. Medicine and science in sports and exercise. 2004;36 (5):807-13.
  19. Percival ME, Martin BJ, Gillen JB, Skelly LE, MacInnis MJ, Green AE, et al. Sodium bicarbonate ingestion augments the increase in PGC-1α mRNA expression during recovery from intense interval exercise in human skeletal muscle. Journal of Applied Physiology. 2015;119 (11):1303-12.
  20. Hollidge-Horvat M, Parolin M, Wong D, Jones N, Heigenhauser G. Effect of induced metabolic alkalosis on human skeletal muscle metabolism during exercise. American Journal of Physiology-Endocrinology And Metabolism. 2000;278 (2):E316-E29.
  21. Ööpik V, Timpmann S, Hackney AC, Kadak K, Medijainen L, Karelson K. Ingestion of sodium citrate suppresses aldosterone level in blood at rest and during exercise. Applied Physiology, Nutrition, and Metabolism. 2010;35 (3):278-85.
  22. Mora-Rodriguez R, Hamouti N. Salt and fluid loading: effects on blood volume and exercise performance. Acute Topics in Sport Nutrition. 2012;59:113-9.
  23. Zhang X, Varin E, Allouche S, Lu Y, Poulain L, Icard P. Effect of citrate on malignant pleural mesothelioma cells: a synergistic effect with cisplatin. Anticancer Research. 2009;29 (4):1249-54.

 

مطالعات کاربردی تندرستی در فیزیولوژی ورزش
دوره 12، شماره 1
فروردین 1404
صفحه 121-135

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  • تاریخ دریافت: 03 اردیبهشت 1403
  • تاریخ بازنگری: 12 مرداد 1403
  • تاریخ پذیرش: 14 مرداد 1403

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