Study Of Selenium On Liver Toxicity Induced By Exposure To Fluoride On Chicken

Fluorine is one of the necessary trace elements for animal body and it has many physiological effects. But if it is ingested excessively over a prolonged period, it will be accumulated in animal body and adversely influence many tissues and organs characterized. As an important detoxifying organ of the body, liver is the main target organ of fluorosis. Among the numerous trace elements which could reduce the toxicity of fluorosis, selenium became a research focus. In this study, 180 Hyline cocks of 8 days old were used as experimental animals. Sodium fluoride and sodium selenium were added to the normal diets in order to duplicate sub-chronic fluorine toxicosis model and antagonism model of selenium to fluorine toxicosis, and to study the effects of selenium on liver toxicity in chiken induced by exposure to fluoride. The results showed as follows:1. Based on the clinic symptom, autopsy, microstructure and ultrastructure observations, it is found that the growth and development of chicken which fed by 1000 mg·kg-1·diet-1 fluoride were cumbered while 4 mg·kg-1·diet-1 of selenium must have a preventive effect in early fluorosis. After the application of selenium, the fluoride poisoning symptoms of chicken relieved. These results revealed that selenium could antagonize the toxicosis of fluorine on the inhibition of growth and development of the chicken and successfully duplicated subchronic-fluorine toxicosis model and antagonism model of selenium to fluorine toxicosis.2. By detecting the activity of GSH-Px and SOD, and the content of MDA, the results revealed that excessive fluorine could induce oxidative stress of liver, destroy antioxidantive defense system, remove the free radical and induced liver damage. Adding selenium to the diet could antagonize the toxicosis of fluorine on the antioxidant system, enhance the antioxidant capacity, reduce the injury of liver.3. By the detection of the activity and contents of cytochrome P450 enzyme system and its relative gene expression, it was revealed that fluorine could affect the contents of cytochrome P450 (CYP450) and cytochrome b5; the activity of NDAPH-CytC, aminopyrine-N-demethylase (AND) erythromycin-N-demethylase (ERND), Aniline-4-hydroxylase (AH); and the expression of CYP450 mRNA. After the application of selenium, the activity and contents of cytochrome P450 enzyme system and gene expression of CYP450 were significantly changed. These results indicated that both cytochrome P450 enzyme system and the oxidative stress of organism participated in the damage of fluorine in liver, and selenium could antagonize the toxicosis of fluorine to liver. 4. The results of TUNEL, DNA gel electrophoresis and the expression of Bcl-2 mRNA which detected by Real Time-FQ-PCR showed that excess fluorine could cause apoptosis in liver, which made the damage of mitochondrion. Adding selenium could relieve the damaging effect of fluorine and could decrease the damaging effect of fluorine on mitochondrion. This may be one machanism of selenium antagonists the apoptosis of liver cell induced by fluorine.In a word, this research successfully duplicated subchronic-fluorine toxicosis model and antagonism model of selenium to fluorine toxicosis, and discussed the toxicity of fluoride and the antagonism of selenium at cell, subcellular and molecular level. It is revealed that selenium could antagonize the toxicity of fluoride at several links. It is also meaningful to prevention and cure fluorosis, to improve the health of animal and ensure the development of graziery.