investigation Histological and biochemical evaluation of pups and liver of ethanol treated pregnancy mothers in rat
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sajjad kooshki,1,* mohammad taghi ghorbanian,2 iran Goudarzi,3 hadis kooshki,4
1. University
2. University
3. University
4. University
- Introduction: In fact, alcohol abuse is a common problem in global health. Excessive alcohol consumption is one of the most effective factors in causing inflammation of the liver (ALD). The effect of alcohol on different tissues depends on the concentration of alcohol in the blood (BAC) depending on how quickly alcohol is absorbed, distributed and metabolized. Continuous alcohol consumption during pregnancy causes serious damage to the developing fetus, the most important consequences of which can be changes in the developing brain and neurobehavioral defects throughout life, as well as leading to a wide range of teratogenic effects. cited. Drinking alcohol, even in moderation, is associated with an increased risk of miscarriage, especially in the first trimester of pregnancy and infertility in women. Ethanol has been shown to be a ligand that induces a death signal to the cell in both in vitro and in vivo conditions, causing programmed death. In animal studies, exposure to alcohol at a stage equivalent to the first trimester of pregnancy in humans caused fetal alcohol syndrome (FAS) and was associated with loss of muscle movement during the second and third trimesters. The third trimester has also been shown to have serious effects on the fetus, as it is associated with a significant increase in essential nutrients in the brain and retina. Frequent consumption of alcohol causes liver dysfunction. Alcohol-induced liver disease is one of the most common causes of liver cancer and cancer mortality, and is also a major cause of leukemia. Ethanol has been shown to cause toxic effects by producing reactive oxygen species (ROS) and inducing lipid peroxidation in various tissues and cells. ROS has been reported to affect the oxidation of proteins, fats. Oxidation damages DNA, inactivating the enzyme and destroying various antioxidant enzymes. These results can cause early stages of liver disease and liver dysfunction. Oxidation of ethanol by the microsomal oxidizing enzyme (cyp2E1) p450 and dihydrogenase causes the accumulation of ROS in the fetal liver. Ethanol-induced liver pathology is associated with cyp2E1 expression. Excessive expression of cyp2E1 causes fat oxidation and oxidative stress in the fetal liver.
The expression level of cyp2E1 in the liver is high because approximately 80% of the ethanol consumed is metabolized in the liver. Ethanol affects MAPKs in cells and systems of different organs, thus showing different pathological effects. Ethanol consumption chronically regulates nitric oxide (NO) levels and the expression level of protein cyclooxygenase (COX) in maternal and neonatal liver tissue. Recent studies by Natabaj have shown that ethanol consumption increases the phosphorylation of jNK, ERK and P38 in the liver of mother and offspring of rat.
- Methods: Pregnant rats were randomly divided into 3 experimental groups: the control group receiving distilled water and the oily ethanol group receiving ethanol with oil by gavage up to 28 days after delivery. Mice in the ethanol group received ethanol (4 g / kg) as a solution in distilled water (40% v / v) as oral gavage from day 0 of gestation until 28 days after delivery. On the 18th day before birth and 28 days after birth, a number of rats were sacrificed for histopathological examination of the liver of the mother and the fetus, and the fetus was examined for weight and appearance. Liver tissue samples were placed at -70 ° C for biochemical tests. And some other animals under deep anesthesia, then perfusion operation was performed and then the animal's liver was removed. For better fixation, we first changed the liver tissue in 10% paraformaldehyde solution every 12 hours and then histopathological examination was performed.
- Results: Evaluation of oxidative enzymes showed a significant increase in MDA in the ethanol group compared to the control group (P <0.5). Also, GPX level decreased significantly compared to control (P <0.05). In histopathology, the number of hepatocytes in the ethanol group increased significantly (P <0.5) and caused hepatocyte necrosis and severe weight loss and fetal defect in the ethanol group.
- Conclusion: According to the results, ethanol caused severe weight loss and defects before and after birth in the pups as well as damage to hepatocytes, Kupffer cells and maternal liver lobules. The number of Kupffer cells decreased.
- Keywords: ethanol, FAS, pups ,pregnancy, rat , liver
