Tez özetleri Astronomi ve Uzay Bilimleri Anabilim Dalı 2


The Effects of Aflatoxin B



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The Effects of Aflatoxin B1 on TM3 Leydig Cells
The purpose of this study is to investigate the effects of aflatoxin B1 by measuring enzymatic antioxidants (catalase, superoxide dismutase), lipid peroxidation, hydrogen peroxide levels, apoptosis and steroidogenic enzyme (3β-hydroxysteroid dehydrogenase, 17β-hydroxysteroid dehydrogenase) levels.

Aflatoxin B1 is one of the most poisonous mycotoxin that produced by fungi as secondary metabolites during harvesting or storage processes of cereals. Consumption of contaminated grains is a global problem that threats the living organisms. Aflatoxin B1 is metabolized by liver and eliminated from the body by kidneys. The remaining portion of aflatoxin B1 accumulates in the body and causes damage in tissues and organs.

Daily intake of contaminated foods leads to constant amount of aflatoxin B1 circulating in blood and seminal fluids. Therefore, it is well known that this steady state can cause severe damage on liver and kidney, along with degeneration, vacuolization in Leydig cells and disrupted steroidogenic activity in testis. Also aflatoxin B1 exposure produces free radicals which can reduce the antioxidant enzyme levels and damage the DNA.

In this study, low (0,3 nM) and high (1,2 nM) aflatoxin B1 concentrations, converted into in vitro conditions from predicted amounts of aflatoxin B1 that are consumed with food were administrated on TM3 Leydig cells for 24 hours. Cell viability, antioxidant and steroidogenic enzymes, lipid peroxidation, hydrogen peroxide levels and apoptotis rate were assayed on following administrations in Leydig cells. The results indicated that antioxidant and steroidogenic enzyme levels are decreased, while cell viability, lipid peroxidation, hydrogen peroxide levels, apoptosis rate are increased in tested groups. These findings suggests that very low doses of aflatoxin B1 can cause oxidative stress in TM3 Leydig cells which leads to apoptosis and may decrease the testosterone levels by inhibition of steroidogenic enzymes.


  

YILDIRIM Gülnaz

Danışman : Prof. Dr. Melike ERKAN

Anabilim Dalı : Biyoloji

Programı : Zooloji

Mezuniyet Yılı : 2014

Tez Savunma Jürisi : Prof. Dr. Melike ERKAN

Prof. Dr. Tuncay ORTA

Prof. Dr. Tülay İREZ

Doç. Dr. Uğur AKSU

Doç. Dr. Meliha İNCELİ




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