Ratlarda deneysel olarak oluşturulan kadmiyum toksikasyonu üzerine likopenin etkilerinin araştırılması
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Tarih
2006
Yazarlar
Dergi Başlığı
Dergi ISSN
Cilt Başlığı
Yayıncı
Hatay Mustafa Kemal Üniversitesi
Erişim Hakkı
info:eu-repo/semantics/closedAccess
Özet
Bu araştırmada, önemli bir çevre kirleticisi olan kadmiyumun böbreklerde oluşturduğu toksikasyon üzerine antioksidan etkili beta-karotenlerden likopenin olası faydalı etkileri deneysel olarak ratlarda araştırıldı. Çalışmada, Wistar cinsi erkek ratlar kontrol, kadmiyum, kadmiyum+likopen ve likopen olmak üzere dört gruba ayrılarak kullanıldı. Kadmiyum, klorür tuzu şeklinde kadmiyum ve kadmiyum+likopen grubu ratlara ağız yoluyla; likopen ise aynı yolla kadmiyum+likopen ve likopen grubu hayvanlara 20 gün süreyle verildi. CdCl2 1/15 LD50 değerine karşılık gelen 6.6 mg/kg/gün, likopen ise 10 mg/kg/gün dozunda verildi. Kan plazması ve böbrek dokusu homojenatlarında lipit perokidasyonu son ürünü malondialdehid ve nitrik oksit düzeyleri; antioksidan enzimlerden süperoksit dismutaz, katalaz ve glutatyon peroksidaz ile oksidan ara ürün oluşturan ksantin oksidaz aktiviteleri spektrofotometrik yöntemle saptandı. Tümör nekroz faktör alfa düzeyi plazma örneklerinde ELISA ile; böbrek dokusu kadmiyum ve çinko seviyeleri ise indüktif olarak eşleşmiş plazma-atomik emisyon spektrofotometre (ICPAES) cihazında ölçüldü. Kadmiyumun ratlarda neden olduğu canlı ağırlık kaybı, plazma ve böbrek dokusunda lipit peroksidasyonu likopen tarafından ortadan kaldırıldı. Plazma nitrik oksit seviyesi hem kadmiyum hem de likopen gruplarında kontrole göre daha düşük olduğu tesbit edildi. Kadmiyumun antioksidan enzimlerden süperoksit dismutaz aktivitesini değiştirmediği, glutatyon peroksidaz aktivitesini azalttığı, katalaz aktivitesinde artışa ve serbest radikal üretici enzim ksantin oksidaz aktivitesinde ise bir değişikliğe neden olmadığı gözlendi. Plazma Tümör nekroz faktör alfa düzeyi üzerine kadmiyum etki göstermedi. Kadmiyum, böbreklerde yüksek miktarlarda birikim gösterirken böbrek dokusu çinko seviyesi üzerine istatistiksel olarak bir etki oluşturmadı. Sonuç olarak, kadmiyum ratlarda şiddetli bir yangı tablosu oluşturmazken, canlı ağırlık kaybı ve oksidatif hasar oluşturmuştur. Kadmiyumun neden olduğu olumsuz etkilerin ise likopen tarafından büyük oranda ortadan kaldırıldığı tesbit edildi.
In this study, the possible benefit of lycopene, an antioxidant beta-carotene, on cadmium [which is an important environmental pollutant] induced kidney toxicity was experimentally studied in rats. Wistar rats were divided into four groups, control, cadmium, cadmium+lycopene and lycopene. Cadmium as chloride salt (CdCl2) was administrated to cadmium and cadmium+lycopene groups by oral route. Lycopene was given to cadmium+lycopene and lycopene groups by the same route for 20 days. The amounth of CdCl2 was calculated by 1/15 LD50 as daily dose (6.6mg/kg daily) and dose of lycopene was 10mg/kg. Lipid peroxidation end product malondialdehyde and nitric oxide concentrations in blood plasma and kidney homogenates, antioxidant enzymes superoxide dismutase, catalase and glutathione peroxidase, and free radical generating enzyme xanthine oxidase activities were determined by spectrometric methods. Plasma tumor necrosis factor alpha levels was analyzed by ELISA. cadmium and zinc levels were measure using inductively coupled plasma atomic emission spectrophotometer (ICP-AES) in kidney tissues. Cadmium caused to reduce live weight and lipid peroxidation in plasma and kidney and these effects were reversed by lycopene administration in rats. Nitric oxide levels were decreased in both cadmium, cadmium+Lycopene and lycopene groups in plasma, respectively. While cadmium did not change antioxidant superoxide dismutase activity, glutathione peroxidase activity was decreased. However, xanthine oxidase activity and plasma tumor necrosis factor alpha concentrations were not altered by cadmium. Cadmium largely accumulated in kidney though it did not statistically modify kidney zinc levels. As a result at this study, cadmium did not cause considerable inflammation according to tumor necrosis factor alpha production, although it induced moderate lipid peroxidation and suppressed some antioxidant enzyme activities, and live weight loss in rats. It was concluded that experimentally administrated lycopene reverse cadmium-caused oxidative stress.
In this study, the possible benefit of lycopene, an antioxidant beta-carotene, on cadmium [which is an important environmental pollutant] induced kidney toxicity was experimentally studied in rats. Wistar rats were divided into four groups, control, cadmium, cadmium+lycopene and lycopene. Cadmium as chloride salt (CdCl2) was administrated to cadmium and cadmium+lycopene groups by oral route. Lycopene was given to cadmium+lycopene and lycopene groups by the same route for 20 days. The amounth of CdCl2 was calculated by 1/15 LD50 as daily dose (6.6mg/kg daily) and dose of lycopene was 10mg/kg. Lipid peroxidation end product malondialdehyde and nitric oxide concentrations in blood plasma and kidney homogenates, antioxidant enzymes superoxide dismutase, catalase and glutathione peroxidase, and free radical generating enzyme xanthine oxidase activities were determined by spectrometric methods. Plasma tumor necrosis factor alpha levels was analyzed by ELISA. cadmium and zinc levels were measure using inductively coupled plasma atomic emission spectrophotometer (ICP-AES) in kidney tissues. Cadmium caused to reduce live weight and lipid peroxidation in plasma and kidney and these effects were reversed by lycopene administration in rats. Nitric oxide levels were decreased in both cadmium, cadmium+Lycopene and lycopene groups in plasma, respectively. While cadmium did not change antioxidant superoxide dismutase activity, glutathione peroxidase activity was decreased. However, xanthine oxidase activity and plasma tumor necrosis factor alpha concentrations were not altered by cadmium. Cadmium largely accumulated in kidney though it did not statistically modify kidney zinc levels. As a result at this study, cadmium did not cause considerable inflammation according to tumor necrosis factor alpha production, although it induced moderate lipid peroxidation and suppressed some antioxidant enzyme activities, and live weight loss in rats. It was concluded that experimentally administrated lycopene reverse cadmium-caused oxidative stress.
Açıklama
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Anahtar Kelimeler
Biyokimya, Biochemistry
