Evaluatıon of Malondialdehyde Level and Paraoxonase 1 Activity in Obese Children

Öz

The high prevalence of childhood obesity and related serious health consequences have received increasing attention in medical studies and health policies. Obesity is recognized as a risk factor for cardiovascular disease. Oxidative stress is a risk factor for endothelial disfunction in obese individuals. Therefore, we aim to evaluate paraoxonase 1 (PON1) activity with malondialdehyde (MDA) levels in obese children.Our study included 51 obese children and 40 healthy controls aged 6-15 years. Obesity was defined as a body mass index (BMI) ≥ 95th percentile for age and gender. While serum lipid profiles were analyzed by Siemens ADVİA 1800, PON1 activity and MDA were evaluated by spectrophotometric method. While triglyceride, total cholesterol and LDL-cholesterol levels were higher, HDL-cholesterol levels were lower in obese children than in controls (p < 0.05). On the other hand, we found that obese children had higher MDA levels and PON1 activities, but this was not significantly different in obese children. Although there is not a significant difference between oxidant and antioxidant parameters in obese children compared with control children, because of dyslipidemia they are recognized as risk factors for cardiovascular disease. Lifestyle changes and entertaining physical activity should be implemented as necessary strategies in managing childhood obesity and dyslipidemia

Anahtar Kelimeler

• Childhood obesity, lipid profiles,BMI, MDA, PON1

OBEZ ÇOCUKLARDA MALONDİALDEHİT SEVİYESİ VE PARAOKSONAZ 1 AKTİVİTESİNİN DEĞERLENDİRİLMESİ

Öz

Çocukluk obezitesi ve ilişkili olduğu ciddi sağlık sorunlarının artan hızı, tıbbi araştırmalarda ve sağlık politikalarında gittikçe daha çok ilgi çekmektedir. Obezite, kardiyovasküler hastalıklar için bir risk faktörü olarak bilinmektedir. Obez kişilerde oksidatif stres, endotel disfonksiyon için bir risk faktörüdür. Bu sebeple çalışmamızda obez çocuklarda paraoksonaz 1 (PON1) aktivitesi ile malondialdehit (MDA) seviyelerinin değerlendirilmesi amaçlanmıştır. Çalışmamıza yaşları 6-15 arasında olan 51 obez ve 40 sağlıklı çocuk alınmıştır. Obezite, yaş ve cinsiyet göz önüne alınarak, 95 persentil ve üzerindeki vücut kitle indeksi (VKİ) ile belirlendi. Serum lipit profili, Siemens ADVİA 1800 ile analiz edilirken, PON1 aktivitesi ve MDA düzeyleri spektrofotometrik metot ile değerlendirildi. Obez çocukların trigliserit, total kolesterol ve LDL-kolesterol seviyeleri kontrol grubundan anlamlı düzeyde yüksek, HDL-kolesterol seviyeleri anlamlı düzeyde düşüktü. Diğer taraftan obez çocuklarda PON1 aktivitesi ve MDA düzeyleri yüksek olmasına rağmen kontrol grubu ile karşılaştırıldığında anlamlı bir faklılık gözlenmedi. karşılaştırıldığı zaman oksidant-antioksidant parametreler açısından anlamlı düzeyde bir farklılık bulunmamasına rağmen, dislipidemi kardiyovasküler hastalıklar için bir risk faktörü olduğu için, çocukluk obezitesinin ve dislipideminin yönetimi için, yaşam biçimi değişiklikleri ve eğlenceli fiziksel aktivite gerekli stratejiler olarak uygulamaya konmalıdır

Anahtar Kelimeler

• Çocukluk obezitesi, lipit profili,VKİ, MDA, PON1

Kaynakça

1. Alemzadeh R, Rising R, Lifshitz F. Pediatric Endocrinology. (5 nd ed.) New York: Marcel Dekker, 2007: 1–26, 211-250.
2. Wethington HR, Sherry B, Polhamus B.Physician practices related to use of BMI-for age and counseling for childhood obesity prevention: a cross-sectional study. BMC Fam Pract 2011: 3; 12–80.
3. Taşan E. Obezitenin tanımı, değerlendirme yöntemleri ve epidemiyolojisi. Türkiye Klinik- leri J Int Med Sci 2005; 1: 1–4.
4. Daniels SR, Arnett DK, Eckel RH, et al. Overweight in children and adolescents: pathophysiology, consequences, prevention, and treatment. Circulation 2005; 111: 1999–
5. Abuja P.M, Albertini R. Methods for monitoring oxidative stress, lipid peroxidation and oxidation resistance of lipoproteins. Clinica Chimica Acta 2001; 306: 1-17.
6. Ayub A, Mackness MI, Arrol S, et al. Serum paraoxonase after myocardial infarction. Arterioscler, Thromb, Vasc Biol 1999; 19: 330 – 335.
7. Mackness MI, Harty D, Bhatnagar D, et al. Serum paraoxonase activity in familial hypercholesterolaemia and insulin dependent diabetes mellitus. Atherosclerosis 1991; 86: – 199.
8. Bundak R, Furman A, Günöz H, et al. Body mass index for Turkish children. Acta Pediatr ; 95: 194–198. Ohkava H, Ohishi N, Yagi K. Assay for lipid peroxides in animal tissues by thiobarbituric acid reaction. Anal Biochem 1978; 95: 351–

9. Eckerson HW, Romson J, Wyte C, et al. The human serum paraoxonase polymorphism: identification of phenotypes by their response to salts. Am J Hum Genet 1983; 35: 214–227.
10. Gupta N, Goel K, Shah P, et al. Childhood obesity in developing countries: epidemiology, determinants, and prevention. Endocr Rev. ; 33: 48-70. Aronne LJ, Nelinson DS, Lillo JL. Obesity as a disease state: A new paradigm for diagnosis and treatment. Clin Cornerstone 2009; 9: 9–
11. Boyd GS, Koenigsberg J, Falkner B, et al. Effect of obesity and high blood pressure on plasma lipid levels in children and adolescents. Pediatrics 2005; 116: 442–446.
12. Reinehr T, Kiess W, de Sousa G, et al. Intima media thickness in childhood obesity: relations to inflammatory marker, glucose metabolism, and blood pressure. Metabolism 2006; 55: 113 –118.
13. Ceriello A, Motz E. Is oxidative stress the pathogenic mechanism underlying insulin resistance, diabetes, and cardiovascular disease? The common soil hypothesis revisited. Arterioscler Thromb Vasc Biol. 2004; 24: 816–
14. Holvoet P, Jenny NS, Schreiner PJ, et al. The relationship between oxidized LDL and other cardiovascular risk factors and subclinical CVD in different ethnic groups: The Multi- Ethnic Study of Atherosclerosis (MESA). Atherosclerosis 2007; 194: 245–252.
15. Harrison D, Griendling KK, Landmesser U, et al. Role of oxidative stress in atherosclerosis. Am J Cardiol. 2003; 91: 7–11.
16. Davi G, Guagnano MT, Ciabattoni G, et al. Platelet activation in obese women: Role of inflammation and oxidant stres. JAMA 2002; : 2008–2014.
17. Yilmaz FM, Yilmaz G, Savas Erdeve S, et al. Serum sialic acid, hs-CRP and oxidative stress parameters in obese children. J Pediatr Endocrinol Metab 2007; 20: 205–210.
18. Karakaya S, El SN, Taş AA. Antioxidant activity of some foods containing phenolic compounds. Int J Food Sci Nutr 2001; 52: 501
19. Meral R, Doğan İS, Kanberoğlu GS. Fonksi- yonel gıda bileşeni olarak antioksidanlar. Iğdır Univ J. Inst Sci & Tech 2012; 2: 45-50.
20. Mackness MI, Mackness B, Durrington PN, et al. Paraoxonase: biochemistry, genetics and relationship to plasma lipoproteins. Curr Opin Lipidol 1996; 7 : 69– 76.
21. Aviram M, Rosenblat M, Bisgaier CL, et al. Paraoxonase inhibits high-density lipoprotein oxidation and preserves its function: a possible peroxidative role for paraoxonase. J Clin Invest 1998;101:1581 –1590.
22. Rozenberg O, Rosenblat M, Coleman R, et al. Paraoxonase (PON1) deficiency is associated with increased macrophage oxidative stress: studies in PON1-knock out mice. Free Radic Biol Med 2003;34: 774– 784.
23. Mackness MI, Arrol S, Abbott C, et al. Protection of low-density lipoprotein against oxidative modification by high density lipoprotein Atherosclerosis 1993; 104:129–135. paraoxonase.
24. Mackness MI, Mackness B, Arrol S, et al. Pre- sence of paraoxonase in human interstitial fluid. FEBS Lett 1997;416:377–380.
25. Garin MC, Kalix B, Morabia A, et al. Small, dense lipoprotein particles and reduced paraoxonase-1 in patients with the metabolic syndrome. J Clin Endocrinol Metab 2005; 90: –2269.
26. Sentı M, Tomas M, Fito M, et al. Antioxidant paraoxonase 1 activity in the metabolic syndrome. J Clin Endocrinol Metab 2003; 88: –5426.
27. Aviram M, Rosenblat M, Billecke S, et al. Human serum paraoxonase (PON1) is inactivated by oxidized low density lipoprotein and preserved by antioxidants. Free Radic Biol Med 1999;26: 892 – 904.
28. Senti M, Tomas M, Vila J, et al. Relationship of age-related myocardial infarction risk and Gln/Arg 192 variants of the human paraoxonase1 gene: the REGICOR study. Atherosclerosis 2001; 156: 443–449.