Protective activity of the methanol extract of Usnea longissima against oxidative damage and genotoxicity caused by afl atoxin $B_1$ in vitro

Amaç: Bu çalışmanın amacı insan kan kültürü hücrelerinde aflatoksin $B_1$ (AF$B_1$) in neden olduğu genotoksisite ve oksidatif stress üzerine /Usnea longissima/ (UME)’dan elde edilen metanolik ekstrakların etkisini araştırmak idi. Yöntem ve gereç: Genotoksik etkilerin tahmini için kardeş kromatid değişimi (SCE) ve mikro nukleus (MN) testleri kullanıldı. Aynı zamanda UME’nin antioksidatif etkisini belirlemek için superoksit dismutaz (SOD) ve glutatyon peroksidaz (GPx) enzimlerinin aktiviteleri ve malondialdehit (MDA) seviyesi ölçüldü. Bulgular: SCE ve MN test sistemlerinde, UME’nin AF$B_1$’in genotoksik etkilerini baskıladığı gözlendi. Ayrıca AF$B_1$ muamelesinden sonra MDA seviyesinde artma, SOD ve GPx enzimlerinin aktivitelerinde azalma gözlendi. UME, AF$B_1$’in neden olduğu bu enzim aktivitelerindeki azalmayı ve lipid peroksidasyonundaki artışı anlamlı düzeyde engellediği görüldü. Sonuç: UME, insan lökosit hücrelerinde AF$B_1$ in neden olduğu SOD ve GPx enzimleri üzerindeki olumsuz etkileri azaltan bir aktivite göstermektedir. Aynı zamanda UME, kuvvetli anti-genotoksik etkiye sahiptir ve UME’nin bu etkisi antioksidant potensiyelinden kaynaklanıyor olabilir.

Usnea longissima metanolik ekstraktının in vitro da afl atoksin $B_1$’in neden olduğu oksidatif stress ve genotoksik etkiye karşı koruyucu etkisi

Aim: To investigate the effects of methanol extracts obtained from Usnea longissima (UME) on the genotoxicity and oxidative stress of aflatoxin B1 (AF$B_1$) in cultured human blood cells. Materials and methods: Sister chromatid exchange (SCE) and micronucleus (MN) tests were used for estimation of genotoxic influences. Activities of superoxide dismutase (SOD) and glutathione peroxidase (GPx) and the malondialdehyde (MDA) level were also measured to evaluate the antioxidative effect of UME. Results: In the SCE and MN test systems, it was observed that UME suppressed the mutagenic effects of AF$B_1$. Furthermore, an increase of MDA level and a decrease of SOD and GPx activities were observed after AFB1 treatment. UME eliminated the genotoxicity of AFB1 and lipid peroxidation by increasing the level of antioxidant enzymes activities. Conclusion: It was shown here for the first time that UME modulates the adverse effects of AF$B_1$ in human blood cells. The results of the present study have also clearly shown that UME has strong antioxidative and antigenotoxic effects, and the role of these enzymes on the mechanism of antigenotoxic activity may be due to its antioxidant potency.

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Turkish Journal of Medical Sciences-Cover
  • ISSN: 1300-0144
  • Yayın Aralığı: Yılda 6 Sayı
  • Yayıncı: TÜBİTAK
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