Sigara ile İndüklenen Böbrek Hasarına Vitamin E ve N-Nitro L-Arginin Metil Esterin (L-NAME) Koruyucu Etkisi
Abstract
Sigara, tütün bitkisinin yapraklarından elde edilen ve
birçok insan tarafından rahatlatıcı etkisi olduğuna inanılan bir maddedir.
Sigara bileşenlerinin, oksidatif stres maruziyeti nedeniyle böbrek fonksiyonu
üzerinde olumsuz etkileri olduğu bilinmektedir. E vitamini organizmayı çeşitli
mekanizmalarla koruyan ve hücresel boyutta hasarı önleyen önemli bir
antioksidan olarak bilinir. L-NAME nitrik oksit (NO) sentaz enzimini inhibe
ederek NO oluşumunu azaltır ve reaktif türlerin neden olduğu oksidatif hasarı
azaltmaya katkıda bulunur. Bu çalışmada, sigara maruziyetinin sıçan böbrekleri
üzerindeki etkisini ve E vitamini ile L-NAME'nin koruyucu etkilerini
araştırmayı amaçladık. Bu amaçla, kırk beş erkek albino sıçan beş gruba
ayrıldı: kontrol, sigara, sigara + E vitamini, sigara + L-NAME, sigara + E
vitamini + L-NAME. Sıçanlar, özel kafeslerde inhalasyon ile sigara dumanına
maruz bırakılmış ve 42 gün boyunca her gün tedavi gruplarına 200 mg/kg BW
Vitamin E ve/veya 50 mg/kg BW L-NAME intraperitoneal olarak uygulanmıştır. 42.
günün sonunda, sıçanların böbrek dokuları ve kanı biyokimyasal ve histolojik
analiz için alındı. Sıçan serumunda kreatinin ve kan üre azotu (BUN) ile böbrek
dokusu homojenatında malondialdehid (MDA), glutatyon (GSH) ve katalaz (CAT)
ölçümleri yapıldı. Sigaraya maruz kalan sıçanlarda serumda kreatinin, BUN ve
dokuda ise MDA düzeyleri anlamlı olarak artmışken, GSH düzeyleri ve CAT
aktivitesi anlamlı olarak azaldı. Serumda kreatinin, BUN, dokuda ise MDA, GSH
düzeyleri ve CAT aktivitesinin tedavi gruplarında normalize olduğu görüldü (p<0.05).
Histolojik incelemeler, tedavi gruplarında iyileşme olduğunu gösterdi. Bu
çalışmada sigara maruziyetinden kaynaklanan böbrek hasarının, E vitamini ve
L-NAME kullanımı ile düzeltilebileceği görülmüştür.
Keywords
References
- Aebi H. 1984. Catalase in vitro. In Methods in Enzymology, 105: 121–126.
- Funck-Brentano C, Raphaël M, Lafontaine M, Arnould JP, Verstuyft C, Lebot M, Roussel R. 2006. Effects of type of smoking (pipe, cigars or cigarettes) on biological indices of tobacco exposure and toxicity. Lung Cancer, 54/1: 11–18.
- Ganafa AA, Socci RR, Eatman D, Silvestrova N, Abukhalaf IK, Bayorh MA. 2002. Acute inhibition of glutathione biosynthesis alters endothelial function and blood pressure in rats. European Journal of Pharmacology, 454/2–3: 217–223.
- Gornall AG, Bardawill CJ, David MM. 1949. Determination of serum proteins by means of the biuret reaction. Journal of Biological Chemistry, 177/2: 751–766.
- Hussain T, Al-Attas OS, Alrokayan SA, Ahmed M, Al-Daghri NM, Al-Ameri S, Sumague TS 2016. Deleterious effects of incense smoke exposure on kidney function and architecture in male albino rats. Inhalation Toxicology, 28/8: 364–373.
- Leonard SW, Bruno RS, Paterson E, Schock BC, Atkinson J, Bray TM, Cross CE, Traber MG 2003. 5-Nitro-γ-tocopherol increases in human plasma exposed to cigarette smoke in vitro and in vivo. Free Radic Biol Med, 35/12: 1560–1567.
- Leone A. 2005. Biochemical markers of cardiovascular damage from tobacco smoke. Current Pharmaceutical Design, 11/17: 2199–2208.
- Modaresi A, Nafar M, Sahraei Z. 2015. Oxidative stress in chronic kidney disease. Iranian Journal of Kidney Diseases, 9/3: 165–179.
- Modlinger PS, Wilcox CS, Aslam S. 2004. Nitric oxide, oxidative stress, and progression of chronic renal failure. In Seminars in Nephrology, 24/4: 354–365.
- Moncada SRMJ, Palmer RML, Higgs EA 1991. Nitric oxide: physiology, pathophysiology, and pharmacology. Pharmacological Reviews, 43/2: 109–142.
- Ohkawa H, Ohishi N, Yagi K. 1979. Assay for lipid peroxides in animal tissues by thiobarbituric acid reaction. Analytical Biochemistry, 95/2: 351–358.
- Saleh S, El‐Demerdash E. 2005. Protective Effects of L‐Arginine against Cisplatin‐Induced Renal Oxidative Stress and Toxicity: Role of Nitric Oxide. Basic & Clinical Pharmacology & Toxicology, 97/2: 91–97.
- Sánchez MH, Vicente LV, Parras FS, Casanova AG, Pescador M, Prieto M, Morales AI. 2016. Oxidative stress role in the development of kidney injury produced by tobacco. Toxicology Letters, 258:255.
- Srivastava SK, Beutler E. 1968. Accurate measurement of oxidized glutathione content of human, rabbit, and rat red blood cells and tissues. Analytical Biochemistry, 25: 70–76.
- Sureshbabu A, Ryter SW, Choi ME. 2015. Oxidative stress and autophagy: crucial modulators of kidney injury. Redox Biology, 4: 208–214.
- Tucker PS, Dalbo VJ, Han T, Kingsley MI. 2013. Clinical and research markers of oxidative stress in chronic kidney disease. Biomarkers, 18/2: 103–115.
- Vaziri ND, Wang XQ, Oveisi F, Rad B. 2000. Induction of oxidative stress by glutathione depletion causes severe hypertension in normal rats. Hypertension, 36/1: 142–146.
- Yeh CC, Barr RG, Powell CA, Mesia-Vela S, Wang Y, Hamade NK, Santella RM. 2008. No effect of cigarette smoking dose on oxidized plasma proteins. Environmental Research, 106/2: 219–225
Protective Effect of Vitamin E and N-Nitro L-Arginine Methyl Ester (L-NAME) on Cigarette Induced Kidney Damage
Abstract
The Cigarette is a material obtained from the leaves of a tobacco plant
and believed to be comforting by many people. Cigarette components are known to
have adverse effects on renal function because of oxidative stress exposure.
Vitamin E is known to be an important antioxidant that protects the organism
with various mechanisms and prevents damage at the cellular dimension. L-NAME
inhibits nitric oxide (NO) synthase, reducing NO formation and contributing to
the reduction of oxidative damage induced by reactive species. In this study,
we aimed to investigate the effects of cigarette exposure on rat kidneys and
protective effect of vitamin E and L-NAME. For this purpose, Forty five male
albino rats were divided into five groups: control, cigarette, cigarette +
vitamin E, cigarette + L-NAME, cigarette + vitamin E + L-NAME. The rats were
exposed to cigarette smoke by inhalation in special cages and 200 mg/kg BW
Vitamin E and/or 50 mg/kg BW L-NAME administered intraperitoneal for 42 days.
These procedures were applied every day. At the end of the 42nd day,
the kidney tissues and blood of rats were taken for biochemical and
histological analysis. Malondialdehyde (MDA), glutathione (GSH) and catalase
(CAT) measurements were performed on the kidney tissue homogenate, creatinine
and blood urea nitrogen (BUN) were measured in the rat serum. While serum
creatinine, BUN and tissue MDA levels significantly increased, GSH levels and
CAT activity decreased significantly in cigarette-exposed rats. Serum
creatinine, BUN, MDA, GSH and CAT levels were normalized in the treatment
groups (p<0.05). Histological examinations showed that there was improvement
in the treatment groups. It has been observed that kidney damage resulting from
cigarette-exposure can be eliminated by the use of vitamin E and L-NAME.
Keywords
References
- Aebi H. 1984. Catalase in vitro. In Methods in Enzymology, 105: 121–126.
- Funck-Brentano C, Raphaël M, Lafontaine M, Arnould JP, Verstuyft C, Lebot M, Roussel R. 2006. Effects of type of smoking (pipe, cigars or cigarettes) on biological indices of tobacco exposure and toxicity. Lung Cancer, 54/1: 11–18.
- Ganafa AA, Socci RR, Eatman D, Silvestrova N, Abukhalaf IK, Bayorh MA. 2002. Acute inhibition of glutathione biosynthesis alters endothelial function and blood pressure in rats. European Journal of Pharmacology, 454/2–3: 217–223.
- Gornall AG, Bardawill CJ, David MM. 1949. Determination of serum proteins by means of the biuret reaction. Journal of Biological Chemistry, 177/2: 751–766.
- Hussain T, Al-Attas OS, Alrokayan SA, Ahmed M, Al-Daghri NM, Al-Ameri S, Sumague TS 2016. Deleterious effects of incense smoke exposure on kidney function and architecture in male albino rats. Inhalation Toxicology, 28/8: 364–373.
- Leonard SW, Bruno RS, Paterson E, Schock BC, Atkinson J, Bray TM, Cross CE, Traber MG 2003. 5-Nitro-γ-tocopherol increases in human plasma exposed to cigarette smoke in vitro and in vivo. Free Radic Biol Med, 35/12: 1560–1567.
- Leone A. 2005. Biochemical markers of cardiovascular damage from tobacco smoke. Current Pharmaceutical Design, 11/17: 2199–2208.
- Modaresi A, Nafar M, Sahraei Z. 2015. Oxidative stress in chronic kidney disease. Iranian Journal of Kidney Diseases, 9/3: 165–179.
- Modlinger PS, Wilcox CS, Aslam S. 2004. Nitric oxide, oxidative stress, and progression of chronic renal failure. In Seminars in Nephrology, 24/4: 354–365.
- Moncada SRMJ, Palmer RML, Higgs EA 1991. Nitric oxide: physiology, pathophysiology, and pharmacology. Pharmacological Reviews, 43/2: 109–142.
- Ohkawa H, Ohishi N, Yagi K. 1979. Assay for lipid peroxides in animal tissues by thiobarbituric acid reaction. Analytical Biochemistry, 95/2: 351–358.
- Saleh S, El‐Demerdash E. 2005. Protective Effects of L‐Arginine against Cisplatin‐Induced Renal Oxidative Stress and Toxicity: Role of Nitric Oxide. Basic & Clinical Pharmacology & Toxicology, 97/2: 91–97.
- Sánchez MH, Vicente LV, Parras FS, Casanova AG, Pescador M, Prieto M, Morales AI. 2016. Oxidative stress role in the development of kidney injury produced by tobacco. Toxicology Letters, 258:255.
- Srivastava SK, Beutler E. 1968. Accurate measurement of oxidized glutathione content of human, rabbit, and rat red blood cells and tissues. Analytical Biochemistry, 25: 70–76.
- Sureshbabu A, Ryter SW, Choi ME. 2015. Oxidative stress and autophagy: crucial modulators of kidney injury. Redox Biology, 4: 208–214.
- Tucker PS, Dalbo VJ, Han T, Kingsley MI. 2013. Clinical and research markers of oxidative stress in chronic kidney disease. Biomarkers, 18/2: 103–115.
- Vaziri ND, Wang XQ, Oveisi F, Rad B. 2000. Induction of oxidative stress by glutathione depletion causes severe hypertension in normal rats. Hypertension, 36/1: 142–146.
- Yeh CC, Barr RG, Powell CA, Mesia-Vela S, Wang Y, Hamade NK, Santella RM. 2008. No effect of cigarette smoking dose on oxidized plasma proteins. Environmental Research, 106/2: 219–225
Details
| Primary Language | English |
|---|---|
| Journal Section | 2018-Articles |
| Authors | |
| Publication Date | June 29, 2018 |
| Acceptance Date | June 28, 2018 |
| Published in Issue | Year 2018 Volume: 3 Issue: 1 |
