Resveratrol Relieved Acute Liver Damage in Ducks (Anas platyrhynchos) Induced by AFB1 via Modulation of Apoptosis and Nrf2 Signaling Pathways

The presence of aflatoxin B1 (AFB1) in feed is a serious threat to livestock and poultry health and to human food safety. Resveratrol (Res) is a polyphenolic compound with antioxidant, anti-apoptotic and other biological activities; however, it is not clear whether it can improve AFB1 induced hepatotoxicity. Therefore, this study was conducted to investigate the effects of dietary Res on liver injury induced by AFB1 and its mechanisms. A total of 270 one-day-old male specific pathogen free (SPF) ducks, with no significant difference in weight, were randomly assigned to three groups: the control group, the AFB1 group and the AFB1 + Res group, which were fed a basic diet, a basic diet and a basic diet containing 500 mg/kg Res, respectively. On the 70th day, the ducks in theAFB1 group and the AFB1+ 500 mg/kg Res group were given 60 μg/kg AFB1 via gavage. When comparing the AFB1 group and the AFB1 + Res group and also with the control group, AFB1 significantly increased liver damage, cytochrome P450 (CYP450) and AFB1-DNA adduct content, increased oxidative stress levels and induced liver apoptosis, which was improved by Res supplementation. In sum, the addition of Res to feed can increase the activity of the II-phase enzyme, activate the nuclear factor E2-related factor 2 (Nrf2) signal pathway, and protect ducks’ livers from the toxicity, oxidative stress and inflammatory reaction induced by AFB1.

Evaluation of the effectiveness of the use of hepatoprotector in acute liver damage by various toxicants in the experiment

Introduction. Acute liver damage with ethanol and its surrogates and chemicals remains an urgent problem. Therefore, studies of the use of hepatoprotector in acute liver damage by various toxicants in the experiment are relevant. The purpose of this study is an experimental evaluation of the use of ademetionine in the early stages of the toxic effects of carbon tetrachloride and ethanol. Materials and methods. The therapeutic effect of the drug “Heptor” in acute intoxication with carbon tetrachloride (subcutaneous administration at a dose of 2 g/kg) and ethanol (oral administration at a dose of 4 g/kg weight) was studied. Studies of metabolic processes in the liver were carried out based on biochemical parameters of rat blood serum. Results. The studies showed that normalization of metabolic processes was observed after introducing “Heptor” against the background of exposure to both toxicants. The therapeutic effect of ademetionine in the case of carbon tetrachloride intoxication had a positive impact after 24 hours of administration and persisted after 72 hours of the experiment. These provisions were based on the results obtained: the restoration of the activity of marker enzymes of hepatocytes (AsAT, AlAT, LDH), the concentration of uric acid and cholesterol, and the indicators of protein metabolism were revealed. The introduction of ademetionine after ethanol intoxication helped restore the function of hepatocytes, which led to the normalization of protein metabolism. The drug stopped hyperenzymemia, which confirmed its membrane-protective properties. Conclusion. “Heptor” has a regenerating, detoxifying and membrane-protective effect in acute liver lesions with carbon tetrachloride and ethanol. The obtained data confirm the universality of this drug, based on the possibility of using various mechanisms of therapeutic action, which allows us to recommend ademetionine as a hepatoprotector to prevent early liver damage when exposed to high doses of multiple toxicants.

Progressive Acute Liver Damage Induced by Repeated 2-Nitropropane: Focused on Obese Mice

Obesity is linked to more deaths worldwide. In obesity, there will be a dysregulation of growth signals such as tumorigenesis. Despite the fact that obesity is tend to progress to acute liver damage, not many study using 2-nitropropane (2NP) as a hepatoxicity agent are undertaken especially in obese mice.This study aimed to determine the regime of 2NP that causes acute liver damage. This is an experimental research using a post-test control design group only, with 3 groups of mice ie O1 (obesity), O2+2-NP1x (induced by 2NP 100 mg/kg BW once), and O2+2-NP2x (induced by 2NP 100 mg/kgBW twice). At 10 weeks, rats were sacrificed and 100 mg liver tissue were collected for MDA, GSH, MnSOD and CAT enzymes analysis. Analysis statistics were performed by SPSS by one-way Anova and post hoc Tukey.MDA levels of mice were found to be increased in 2NP group than control (3.768 ± 0.407 nmol/mg) (p < 0,01). Liver GSH, MnSOD and CAT levels of both single injection 2-NP and repeated injection 2-NP groups decreased compared to those of controls (p<0,01). Repeated injection of 2-NP worsen the acute liver damage in obese mice.

Long-term therapy with non-steroidal anti-inflammatory drugs for axial spondyloarthritis: focus on changes in liver function

The purpose of the study is to analyze the state of liver function in patients with spondyloarthritis taking non-steroidal anti-inflammatory drugs continuously for 24 months. Materials and methods of the study include 198 patients with spondyloarthritis. The prospective study involved 36 patients with spondyloarthritis who took non-steroidal anti-inflammatory drugs (NSAIDs) prescribed by a physician in the community for 24 months. The level of liver enzymes in blood serum at admission and in dynamics was studied. The increase of liver enzymes was detected in 12 (6.06%) of 198 patients with spondyloarthritis. Among them 6 (50%) patients took methotrexate, 1 (8.33%) - genetically engineered drug, 2 (16.67%) patients-sulfasalazine and 3 (25%) - nonsteroidal anti - inflammatory drugs. 19.4% of patients were registered with a periodic increase of transaminase levels on the background of NSAIDs for the last 24 months. At the same time, no cases of acute liver damage or progressive deterioration of liver function requiring discontinuation of therapy were recorded during the entire follow-up period.

Acute liver damage in Hyperemesis gravidarum — case report

Hyperemesis gravidarum (HG) involves severe, persistent, intractable nausea and vomiting, which subsequently leads to weight loss>5% of weight until pregnancy, in the absence of other causes, accompanied by dehydration, nutritional deficiency with ketosis, abnormalities electrolyte and/or acid-base balance disorders. in the paper we present the case of a 26-year-old woman, G2N1, in week 10 of gestation, who developed in the context of HG severe abnormalities, namely acute liver damage, with hepatopriv syndrome (Prothrombin after Quick 53%, INR -1, 42, total protein 46.91 /l, cholestatic syndrome (total bilirubin 39 mcmol/l) and cytolytic syndrome (ALT — 140.25 IU / L and AST -125.42 IU / L); alkalemia (arterial pH 7.51) , hyponatremia (serum sodium 132 mmol/l), hypokalemia (serum potassium 2.72 mmol/l). The diagnosis of HG, complicated by acute liver failure, has been confirmed. All laboratory symptoms and abnormalities were resolved by targeted administration of intravenous fluids, antiemetic treatment, and prophylactic antithrombotic treatment.

Acute liver injury following acetaminophen administration does not activate atrophic pathways in the mouse diaphragm

N-acetyl-para-amino phenol (APAP, usually named paracetamol), which is commonly used for its analgesic and antipyretic properties may lead to hepatotoxicity and acute liver damage in case of overdoses. Released cytokines and oxidative stress following acute liver damage may affect other organs’ function notably the diaphragm, which is particularly sensitive to oxidative stress and circulating cytokines. We addressed this issue in a mouse model of acute liver injury induced by administration of APAP. C57BL/6J mice (each n = 8) were treated with N-acetyl-para-amino phenol (APAP) to induce acute drug caused liver injury and sacrificed 12 or 24 h afterwards. An untreated group served as controls. Key markers of inflammation, proteolysis, autophagy and oxidative stress were measured in diaphragm samples. In APAP treated animals, liver damage was proven by the enhanced serum levels of alanine aminotransferase and aspartate aminotransferase. In the diaphragm, besides a significant increase in IL 6 and lipid peroxidation, no changes were observed in key markers of the proteolytic, and autophagy signaling pathways, other inflammatory markers and fiber dimensions. The first 24 h of acute liver damage did not impair diaphragm atrophic pathways although it slightly enhanced IL-6 and lipid peroxidation. Whether longer exposure might affect the diaphragm needs to be addressed in future experiments.