RESEARCH PAPER
Immunohistochemical evaluation of the influence of L-arginine on biomarkers of environmental (cellular) stress in the kidneys of pregnant female rats
| 1 | Department of Histology and Embryology medical University in Lublin, Poland |
| 2 | Department of Maritime and Hyperbaric Medicine Military Institute of Medicine, Gdynia, Poland |
CORRESPONDING AUTHOR
Ann Agric Environ Med. 2017;24(1):121–128
KEYWORDS
ABSTRACT
Introduction:
Kidney damage during pregnancy constitutes a diagnostic and therapeutic challenge. However, it is not entirely known whether a kidney condition recognised before the pregnancy releases an organism’s response to pregnancy, or whether pregnancy itself worsens kidney function.
Objective:
The aim of the study was immunohistochemical evaluation of cells of kidneys of pregnant rats under the influence of nitric oxide (NO), with measurement of the immunoexpression of cellular stress markers (p-53, HSP 70). The dose of administered L-arginine (NO substrate) was approximated to that applied in obstetrics in gestosis prevention and treatment in pregnant women.
Material and Methods:
60 female rats used in experiment were divided into 6 groups: 3 experimental and 3 control. The females from experimental groups were administered L-arginine (40g/kg, per os) every other day starting from the seventh day or pregnancy. The animals were decapitated on the 10th, 20th day of pregnancy, and 10 days after the delivery. Kidneys taken from decapitated rats were evaluated using the immunohistochemical three step method. HSP 70 and p-53 proteins were detected.
Conclusions:
L-arginine increased the expression of p-53 protein – on the 10th day of pregnancy, which increased at the end of pregnancy; however, 10 days after delivery the level dropped below that observable during physiological pregnancy. Hormonal changes in physiological pregnancy cause an increase in expression of the p-53 (cell stress marker) in the epithelial cells of renal tubules, mainly at the end of pregnancy (20th day). 10 days after the delivery, this expression decreases. The expression of HSP-70 protein increases already on the 10th day of pregnancy and maintains a similar level throughout the pregnancy, but is reduced after the puerperium.
Kidney damage during pregnancy constitutes a diagnostic and therapeutic challenge. However, it is not entirely known whether a kidney condition recognised before the pregnancy releases an organism’s response to pregnancy, or whether pregnancy itself worsens kidney function.
Objective:
The aim of the study was immunohistochemical evaluation of cells of kidneys of pregnant rats under the influence of nitric oxide (NO), with measurement of the immunoexpression of cellular stress markers (p-53, HSP 70). The dose of administered L-arginine (NO substrate) was approximated to that applied in obstetrics in gestosis prevention and treatment in pregnant women.
Material and Methods:
60 female rats used in experiment were divided into 6 groups: 3 experimental and 3 control. The females from experimental groups were administered L-arginine (40g/kg, per os) every other day starting from the seventh day or pregnancy. The animals were decapitated on the 10th, 20th day of pregnancy, and 10 days after the delivery. Kidneys taken from decapitated rats were evaluated using the immunohistochemical three step method. HSP 70 and p-53 proteins were detected.
Conclusions:
L-arginine increased the expression of p-53 protein – on the 10th day of pregnancy, which increased at the end of pregnancy; however, 10 days after delivery the level dropped below that observable during physiological pregnancy. Hormonal changes in physiological pregnancy cause an increase in expression of the p-53 (cell stress marker) in the epithelial cells of renal tubules, mainly at the end of pregnancy (20th day). 10 days after the delivery, this expression decreases. The expression of HSP-70 protein increases already on the 10th day of pregnancy and maintains a similar level throughout the pregnancy, but is reduced after the puerperium.
REFERENCES (27)
2.
Haupt S, Beraer M, Goldberg Z, Haupt Y. Apoptosis-the p53 network. J Cell Sci. 2003; 116: 4077–4085.
3.
Ramaglia V, Buck LT. Time-dependent expression of heat shock proteins 70 and 90 in tissues of the anoxic western painted turtle. J Exp Biol. 2004; 207: 3775–3784.
4.
Grudniak AM, Kuć M, Wolska KI. Role of Escherichia coli DnaK and DnaJ chaperones in spontaneous and induced mutagenesis and their effect on UmuC stability. FEMS Microbiol Lett. 2005; 242: 361–366.
5.
Smith O. Cancer. Nota bene: The killer instinct of a p53 target. Science. 2000; 290: 67.
6.
Yoo JL, Janz DM. Tissue-specyfic HSP 70 levels and reproductive physiological responses in fishes inhabiting a metal-contaminated creek. Arch Environ Contam Toxicol. 2003; 45: 110–120.
7.
Evans TG, Yamamoto Y, Jeffery WR, Krone PH. Zebrafish Hsp 70 is required for embryonic lens formation. Cell Stress Chaperones. 2005; 10: 66–78.
8.
Hsu YL, Kuo PL, Tzeng WS, Lin CC. Chalcone inhibits the proliferation of human breast cancer cell by blocking cell cycle progression and inducing apoptosis. Food Chem Toxicol. 2006; 44: 704–713.
9.
Chmielewski M, Linke K, Zabel M, Szuber L. Apoptosis in the liver. Gastroent Pol. 2003; 10: 453–462.
10.
Guicciardi ME, Gores GJ. AIP1: a new player in TNF signaling. J Clin Invest. 2003; 111: 1813–1815.
11.
Djukic M, Jovanovic MD, Ninkovic M, Stevanovic I, Curcic M, Topic A, Vujanovic D, Djurdjevic D. Intrastriatal pre-treatment with L-NAME protects rats from diquat neurotoxcity. Ann Agric Environ Med. 2012; 19: 666–672.
13.
Malyshev IYu, Bayda LA, Trifonov AI, Larionov NP, Kubrina LD, Mikoyan VD, Vanin AF, Manukhina EB. Cross-talk between nitric oxide and HSP70 in the antihypotensive effect of adaptation to heat. Physiol Res. 2000; 49: 99–105.
14.
Harris MB, Blackstone MA, Ju H, Venema VJ, Venema RC. Heat-induced increases in endothelial NO synthase expression and activity and endothelial NO release. Am J Physiol Heart Circ Physiol. 2003; 285: H333-H340.
15.
Mohanty S, Sahu PK. Evaluation of oxidative stress in pregnancy induced hypertension. J Clin Biochem. 2006; 21: 101–105.
16.
Biesiak L, Pietrzak Z, Brocka U. Some factors of oxidative stress in pregnancy with preeclampsia and cholestasis Gin Pol. 2007; 78: 956–960.
17.
Rytlewski K, Zdebski T. Nitric oxide as a mechanism covering pregnancy. Gin Pol. 2001; 72: 758–743.
18.
Pokrovskiĭ MV, Pokrovskaia TG, Gureev VV, Barsuk AA, Proskuriakova EV, Korokin MV, Gudyrev OS, Belous AS, Kochkarov VI, Danilenko LM, Levashova OV, Mal’tseva NV, Polianskaia OS. Correction of endothelial dysfunction by L-arginine under experimental preeclampsia conditions. Eksp Klin Farmakol. 2012; 75: 14–16.
19.
Manitus J. From organogenesis to chronic renal failure and hypertension. Post Nauk Med. 2009; 10: 744–750.
20.
Morris JM, Algert CS, Falster MO, Ford JB, Kinnear A, Nicholl MC, Roberts CL. Trends in planned early birth: a population-based study. Am J Obstet Gynecol. 2012; 207: 186–188.
21.
Nelson SH, Steinsland OS, Wang Y, Yallampalli C, Dong YL, Sanchez JM. Increased nitric oxide synthase activity and expression in the human uterine artery during pregnancy. Circ Res. 2000; 87: 406–411.
22.
Evans RW, Fernstrom JD, Thompson J, Morris SM Jr, Kuller LH. Biochemical responses of healthy subjects during dietary supplementation with L-arginine. J Nutr Biochem. 2004; 15: 534–539.
23.
Rytlewski K, Olszanecki R, Korbut R, Zdebski Z. Effects of prolonged oral supplementation with l-arginine on blood pressure and nitric oxide synthesis in preeclampsia. Eur J Clin Invest. 2005; 35: 32–37.
24.
Facchinetti F, Longo M, Piccinini F, Neri I, Volpe A. L-arginine infusion reduces blood pressure in preeclamptic women through nitric oxide release. J Soc Gynecol Investig. 1999; 6: 202–207.
25.
Gupta V, Gupta A, Saggu S, Divekar HM, Grover SK, Kumar R. Anti-stress and Adaptogenic Activity of l-Arginine Supplementation. Evid Based Complement Alternat Med. 2005; 2: 93–97.
26.
Neri I, Blasi I, Facchinetti F. Effects of acute L-arginine infusion on non-stress test in hypertensive pregnant women. J Matern Fetal Neonatal Med. 2004; 16: 23–26.
27.
Hashimoto S, Takahashi K, Amiel D, Coutts RD, Lotz M. Chondrocyte apoptosis and nitric oxide production during experimentally induced osteoarthritis. Arthritis Rheum. 1998; 41: 1266–1274.
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