Determination of Biochemical and Histological Parameters of Alcohol Administration in Wistar Rats (original) (raw)
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MODULATORY EFFECTS OF CHRONIC ETHANOL INGESTION ON HEPATOTOXICITY-RELATED PARAMETERS IN MALE RATS
5 g o ethanol (20% w/v) per kg body weight was administered to ten rats weighing between 166 – 170 grams daily for 28 days along side with normal feeds and water ad libitum. The administration of ethanol was done orally using oral catheter. A control group o ten rats was set up for a proper experimental evaluation. Analysis at the end of the admin stration showed tha ethanol in a dose of 5g/kg body weight significantly modulates (P<0.05) the activities of selected liver enzymes: alanine amino transferase (ALT), aspartate amino transferase (AST), gamma glutamyl transferase (GGT) and alkaline phosphatase (ALP) as well as those of selected antioxidant enzymes: catalase (CAT) and superoxide dismutase (SOD). f f i t
Liver histology of Wistar rats (Rattus norvegicus) following oral administration of 50% ethanol
Journal of Sustainability Science and Technology, 2022
ARTICLE INFO Ethanol, also known as ethyl alcohol, pure alcohol, and alcohol, is a toxic, volatile, flammable, and colorless liquid. Alcohol is the most commonly consumed alcoholic beverage in everyday life. EtOH is a common abbreviation for ethanol, where "Et" stands for the ethyl group (C2H5). Sugar fermentation to ethanol is one of the earliest organic reactions ever performed by humans; ethanol consumption has also been known for a very long time. This study aims to determine the histology of the liver in Wistar rats (Rattus norvegicus) by orally administering ethanol at a concentration of 50 percent. The method used in this study was an experimental study by looking at the histology of rat liver. Rats were divided into two groups, with seven rats each. Group 1 was given 50% ethanol orally for seven days, and group 2, as a control, was only given orally with distilled water. After seven days, the rats were slaughtered, and their livers were extracted for further histological preparations. In the histology results of group 1, the histological images of the livers of the rats P1, P2, P3, P4, P5, P6 and P7 were abnormal or damaged. In the presence of necrotic cells, oral administration of 50 percent alcohol causes damage to hepatocyte cells, as determined by the study's findings. However, in general, hepatocyte cell damage in the liver produces a score of 1.7, which indicates a change leading to cell damage.
ABSTRACT Though classified as a depressant, the amount of alcohol consumed often determines the end effect. However, little or no existing record(s) relays this effect on the activity of the gastrointestinal tract. Hitherto was current study undertaken to investigate the acute effects of a relatively large dose of alcohol on the small intestine in wistar rats. Thirty (30) male Albino rats of between 138g and 185g were procured from the breeding colony of the Animal House Division of Emma-Maria Biomedic Laboratories and Consultancy, Abraka, Delta state. The animals were then transported (in plastic baskets) to the Animal House of the Faculty of Basic Medical Sciences, Delta state University, Abraka where they were acclimatized for ten days at 28 ± 2ºC, relative humidity 60-70 % and 12hr light/ dark cycle. During study period, animals were supplied with standard grower mash diet (Composition of the grower‘s marsh: Protein -19.0% Fat -2.85% Fibre -6.00% Calcium -1.00% and phosphate -0.45% Energy -2875 KGC) and water ad libitum, in standard wire meshed wooden cages for 10 days prior to commencement of the experiment, following which they were grouped into; Group I (control group), which received normal feed and water ad libitum for 31, 61 and 91days respectively. Group II (Experimental) rats received 7% alcohol with normal feed and water ad libitum for 31, 61 and 91days respectively. For each treatment per week, animals‘ weights were determined and recorded with the electronic weighing balance every 7 days (weekly). Following period of administration, animals were sacrificed by cervical dislocation and blood samples collected by cardiac puncture, assayed and compared in each rat (with control). In each case, photomicrograph of the small intestine was also obtained, whilst comparing histo-architectural changes. Upon statistical comparison (using the student t-test), study found alcohol to cause a statistically significant decrease in body weights across groups, with an increase in antioxidant enzyme activities in the small intestine. KEYWORDS: Alcohol, Small Intestine, antioxidant
Acta Pharmacologica et Toxicologica, 2009
Male Wistar rats were given ethanol chronically (20-30% of the energy as ethanol) in a nutritionally sufficient regimen. Controls received lipid as isoenergetic substitute for ethanol. Treatment lasted for 2 or 8 weeks. Hepatic protein synthesis was measured in fasted rats during a 32 min. continuous infusion of 'H-valine. After 2 weeks of treatment accumulation of hepatic protein was observed in the ethanol group, but there was no change in hepatic protein synthesis or morphology. After 8 weeks the rate of hepatic protein synthesis was decreased by 35% in the ethanol group, but there was no accumulation of protein and a slight accumulation of intracellular lipid droplets. Neither the subcellular distribution of incorporated 'H-valine, nor the activities and distributions of alcohol dehydrogenase and NADPH cytochrome c reductase were changed. Mitochrondrial cytochrome c oxidase activity was decreased in the ethanol group, and cytosolic and microsomal fractions showed higher cytochrome c oxidase activity in this group. Chronic ethanol treatment for 8 weeks had an adverse effect on general protein synthesis as well as on a specific enzyme in the liver in the absence of serious morphologic abnormalities.
Gastroenterology, 2002
Background & Aims: Rats fed ethanol at a constant rate through a permanent intragastric cannula have a regular fluctuation in blood alcohol level (BAL) and urine alcohol level (UAL). The level of ethanol peaks every 6 -10 days. The question is how the liver differs at the peaks and troughs of the UAL cycle. Hypoxic injury is postulated to occur at the peaks. Therefore, liver injury may be different at the peaks and troughs. Methods: Many parameters were measured at the peaks, troughs, and controls for comparison. Results: Indicators of hypoxic injury at the peaks included ATP reduction, a shift to the reduced state in the NADH/NAD ratio, an increase in expression of vascular endothelial growth factor, an increase in the pathology score at the peaks, and an increase in adduct formation using pimonidazole. Liver nitrites, number of granulocytes, liver weight/body weight ratio, cytochrome P450 2E1 protein, and chymotrypsin-like activity changed in the same direction compared with control values. Conclusions: The results indicate that hypoxic injury occurs at the peaks. There was a marked shift in NADH/NAD redox state at the peaks caused by hypoxia. This shift could account for the reduced rate of ethanol elimination by alcohol dehydrogenase at the peaks.
Effect of Chronic High Dose-Alcohol Consumption on the General Biochemical Parameters
2009
Objectives: A chronic intake of high dose alcohol may cause oxidative stress, meta- bolic abnormalities and nutritional deficiencies in the body. The effect of long-term alcohol consumption on the biochemical parameters has not been explained well. Materials and Methods: Female and male rats were maintained for 90 days as follow: I. Control (n=7), II. Alcohol-treated (2.5 gr of 50% ethanol/kg
Ethanol-Induced Hepatopathy in Rats
A chronic consumption of alcohol can lead to the generation of oxygen free radicals and reactive aldehydic species which alter the activities of lysosomes. Furthermore, the reduction in protein degradation contributes to excessive protein accumulation.This was associated with reduced volume densities of autophagosomes and autolysosomes, as determined morphometrically. In this respect the current study was endevoured to the detection of the oxidative stress (serum MDA) as well as the liver tissue homogenate enzymes as arylsulphatase A, Aryl sulphatase B, B-glucoronidase, in addition to the liver histopathological examination of alcohol fed rat livers showed histopathological changes. These findings confirmed the biochemical results which demonstrated that the ingestion of alcohol to rats induced oxidative stress or which was manifested by the strikingly significantly increase in the level of serum MDA associated with significant decrease in the hepatic specific enzymatic activities o...
Clinics in Dermatology, 1999
A lcohol is a small molecule that is both water and lipid soluble. Therefore, it readily permeates all organs of the body and affects many of their vital functions. The most important ones, the likely mechanisms, as well as associated alcohol-drug interactions will be reviewed, with only brief mention of the classic, well-documented cutaneous signs of alcoholism and some newer emerging associations, which are discussed in detail elsewhere in this issue.
Animal Models of Alcoholic Liver Disease for Hepatoprotective Activity Evaluation
BIO Web of Conferences, 2021
Background: The reported statistics suggest that alcoholic liver disease is on the rise. Furthermore, medications used to treat the disease have unpleasant effects, and this necessitates the need to continuously investigate hepatoprotective agents. This study investigates animal models of alcoholic liver disease used to evaluate hepatoprotective activity. Content: A good number of published articles evaluating hepatoprotective activity were summarized. The studies used three ethanol-induced liver injury models: the acute ethanol-induced liver injury model, the chronic ethanol-induced liver injury model, and Lieber– DeCarli model. Summary: Wistar rats were primarily used in the ethanol-induced liver injury model. High levels of alanine transaminase (ALT) and aspartate transaminase (AST) and histopathological alterations were found in all animal models (acute ethanol-induced liver injury, chronic ethanol-induced liver injury, and Lieber–DeCarli models). Severe steatosis was shown in b...
Effects of chronic ethanol consumption in blood: A time dependent study on rat
Indian Journal of Clinical Biochemistry, 2009
Alcohol consumption and health outcomes are complex and multidimensional. Ethanol (1.6g / kg body weight/ day) exposure initially affects liver function followed by renal function of 16-18 week-old male albino rats of Wistar strain weighing 200-220 g. Chronic ethanol ingestion increased in thiobarbituric acid reactive substances level and glutathione s-transferase activity; while decreased reduced gluatathione content and activities of catalase, glutathione peroxidase and glutathione reductase in a time dependent manner in the hemolysate. Though superoxide dismutase activity increased initially might be due to adaptive response, but decreased later. Elevation of serum nitrite level and transforming growth factor-b 1 activity indicated that long-term ethanol consumption may cause hepatic fibrosis and can elicit pro-angiogenic factors. However, no alteration in vascular endothelial growth factor-C activity indicated that ethanol consumption is not associated with lymphangiogenesis. Therefore, we conclude that long-term ethanol-induced toxicity is linked to an oxidative stress, which may aggravate to fibrosis and elevate pro-angiogenic factors, but not associated with lymphangiogenesis.