SİSTEMİK SKLEROZDA OKSİDATİF STRES

Abstract

Sistemik skleroz (SSc), bağ dokusunun kan damarlarında, deride, sinoviumda, iskelet kasında ve gastrointestinal sistem, akciğerler, kalp ve böbrekler gibi bazı iç organlarda infla-masyon, fibrozis ve dejeneratif değişikliklere yol açan kronik bir hastalığıdır. Sistemik sklerozun etyopatogenezi iyi bilinmemektedir ve başlangıç dönemindeki endotel hasarında oksidatif stresin rol oynadığı düşünülmektedir. Son 10 yıl içinde in vitro ve in vivo yapılan çalışmalarda da, aşırı serbest radikal üretiminin, sistemik skleroz patofizyolojisinde rol oynadığı gösterilmiştir. Endotel hücrelerinin fonksiyonel bozukluğu en çok hastalığın erken dönemlerinde ortaya çıkar. İskeminin kendisi özellikle de hipoksiyle birlikteyse doku hasarına neden olabilir. Aktive olmuş oksijen türevleri, hasarı hem başlatıp her de ilerlemesine neden olurlar. Bunlar arasında hipoksantin-ksantin oksidaz sistemi, bozulmuş mitokondrial elektron transport sistemi, aktive olmuş polimorfonük-leer lökositler(PMNL)’ler ve lipoksijenaz yoluyla araşidonik asit metabolizması vardır. Sistemik sklerozda Raynaud Fenomeni, proliferatif okluzif vasküler hastalıkla ve sonuçta serbest oksijen radikallerinde artışla ve doku hasarıyla ilişkilidir. İnflamatuvar hücrelerin ve oksidatif hasar biyo-markırlarının aktivasyonu, iskemik atakların daha sık olduğu ve daha fazla sağlam dokunun bulunduğu, hastalığın erken döneminde daha fazladır. Vasküler hastalık, metabolik yolları uyararak oksidatif stresi artırabilir. Dr. Şükran ERTEN, Dr. Murat TURGAY

Keywords

• Sistemik skleroz
• oksidatif stress
• antioksidan.

OXIDATIVE STRESS IN SYSTEMIC SCLEROSIS

Abstract

SSc is a chronic disease of connective tissue causing inflammation, fibrosis and degenerative changes of blood vessels, skin, synovium, skeletal muscle and internal organs like gastrointestinal system , lungs, heart and the kidneys. Etiopathogenesis of the systemic sclerosis is not well known and oxidative stres has been thought to play a role on endothelial damage at early stages of the disease. It was also shown by in vivo and in vitro studies in last ten years that exess free radical production plays a role in pathophysiology of SSc. Functional dysfunction of endothelial cells is mostly seen at early stages of the disease. Ischemia can cause tissue damage especially when it is together with hypoxia. Activated oxygen derivatives both initiate and promote ishemic tissue damage. These include hypoxanthine-xanthin oxidase system, impaired mitochondrial electron transport sytem, activated PMNLs and arachidonic acid mechanism by lipoxygenase pathway. Raynaud phenomenon is associated with proliferative vascular occlusive disease and ultimately increase in oxygen free radicals and tissue damage. Activation of inflammatory cells and oxidative damage biomarkers is much more pronounced at early stages of the disease where there is more intact tissue. Vascular damage may accelerate oxidative stress by stimulating methabolic pathways.

Keywords

• Systemic sclerosis
• oxidative stress
• antioxidants

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