Bakcground & Aims: Mice models as in-vivo model for cancer research provide significant help to researchers about the mechanisms of tumorigenesis in dynamic systems which affected by many factors such as hormones, various cellular communications, diets, and chemicals. One of the most common cancer is hepatocarcinoma or liver cell cancer, which has different stages and caused by various environmental and genetical factors. THIOACETAMIDE is a kind of toxin which destroys liver tissue through affects the mechanisms of cell proliferation, differentiation and apoptosis by the destruction or damage of cell structure induction pathways, increasing the risk of genetic errors and stimulating the evolution of cells into malignant neoplasia, and is used in many industries such as leather, textile, paper and rubber, but its carcinogenic mechanisms are not well defined. In order to diagnose liver cancer, there are various methods including liver function test such as ALT (alanine aminotransferase), AST (aspartate aminotransferase), ALP (alkaline phosphatase), GGT (Gamma glutamyl transferase) and tumor markers such as CEA (Carcinoembryonic Antigen) and AFP (Alpha fetoprotein), which are most widely used prognosticators for determining cancer, but their specificity and sensitivity is not high. Therefore, the direct method of examining the tissue, pathology method is used for the final diagnosis of cancer. It shows the structural changes of the cells. In this study, by using the in-vivo modeling of cancer in mice exposed to a toxic substance, we have investigated different stages of hepatocarcinogenesis process, in order to help doctors to have in-vivo samples at every stage of the occurrence of this cancer for treatment purposes and to make decisions about how to treat and test different drugs. Methods: In this research, in order to determine the tolerance and lethal dose of THIOACETAMIDE, before starting the main experiment, 18 male mice in 3 groups of 6 were treated for 4 months with different doses of THIOACETAMIDE including 100, 200 and 300 mg/L respectively and after observing the process of mortality, causing shock, lethargy and investigating the cause of death after surgery in different groups, the best dose was determined. More than half of the mice in the high-dose group were shock and died in less than a month, while in the low-dose group, the tissues were still healthy after surgery and just in the middle dose receiver mice, the tissue changes was obtained, which was precisely determined during the main test by examining the pathology of the changes. After determining the carcinogenic concentration of THIOACETAMIDE, in this study, 200 mg/L (equivalent to 33 mg/l daily TAA) of THIOACETAMIDE was consumed as a solution in drinking water to make liver cancer in mice. Mice were euthanized by ketamine/xylazine after 2 and 4 months. Then the livers of mice were separate in formalin to investigate the cancer process. After staining with Hematoxylin/Eosin, the tissue samples were studied using a light microscope with different magnifications by a camera installed on the microscope and a computer system connected to the camera with DINO CAPTURE software. Results: Liver samples were examined in terms of morphology, cytoplasmic staining, nuclear size and cellular atypia (abnormality and uniformity of cells). Also, for staging in case of cancer, the size of tumors, the number of lymph nodes containing tumor and the rate of spread (metastasis) were investigated. No histopathological lesion was observed in the samples taken from the liver of the control group and the liver had a normal structure. Among the tissue lesions created in the group that were euthanized after 2 months, we can mention mild to moderate dysplasia, which is associated with hypertrophy (enlargement) of liver cell nuclei, bordering of nuclei, degeneration of some cells, and swelling of cell walls. Also, in some areas, the expansion of diss space and sinusoid can be seen. The liver tissue of mice exposed to THIOACETAMIDE for 4 months is completely necrotic. Hepatic lobules and dysplastic hepatic portal space can be seen and focal structural changes are also observed. Many necrotic foci are seen in the liver, which indicates the destructive effect of THIOACETAMIDE in acute liver damage. Hepatic lobules and dysplastic hepatic portal space can be seen and focal structural changes are also observed. Many necrotic foci are seen in the liver, which indicates the destructive effect of THIOACETAMIDE in acute liver damage. Conclusion: In vivo mice models are key tools for oncology, pharmaceutical, genetics and other research studies. Considering that nearly five hundred thousand patients are diagnosed with liver cancer every year and it is associated with a poor prognosis, therefore creating experimental models to define the pathogenesis of HCC that occurs in the early stages of liver cancer can be a solution in the direction of reduce the cost of cancer research. Our results showed that THIOACETAMIDE as an organosulfur can change the structure of liver cells and severely inflame the tissue during 4 months. THIOACETAMIDE leading to apoptosis and necrosis of these cells by CYP2E1 enzymes present in liver microsomes through the mechanism of oxidation to THIOACETAMIDE S-oxide, which changes the permeability of cells, increases intracellular calcium concentration, increases nuclear volume and inhibits mitochondrial activity by reducing their membrane potential in liver cells. TAA has long been recognized as a hepatotoxin that requires biological activation of S oxidation to THIOACETAMIDE oxide (TASO) and then to the highly reactive S-Oxide (TASO2) and can be tautomerized to acyl species which capable of transforming cellular nucleophiles include phosphatidylethanolamine (PE) lipids and proteins with lysine side chains. Liver cells can effectively oxidize TA to TASO and TA make strongly covalent bonds with lipids and proteins. Exposure to this substance can activate the ROS system (reactive oxygen species) such as nitric oxide (NO), which causes cell death due to interaction with superoxidase ion and the formation of peroxynitrite, which causes a significant decrease in FRAP values, which indicates the capacity of antioxidant. It can also affect the pre-apoptotic signaling pathways through G protein-coupled receptors, as well as the effect on the phosphorylation of the transcription factor P53, the production of inflammatory cytokines such as NF-kB, the metabolism and apoptosis of cells. In this project, after 2 months of exposure the mice to THIOACETAMIDE, liver tissue cells gradually changed towards fibrosis and after 4 months, some cells changed to necrosis, which indicates the irreversible effects of this substance in the body. In conclusion, it seems that mice model has the potential to be used as accessible strategies replace human samples.

The electron transport layer plays a pivotal role in shaping the photovoltaic attributes of perovskite solar cells. SnO2 stands out as an exemplary electron transport layer for perovskite solar cells due to its exceptional carrier mobility, deep conduction band, suitable band gap, and compatibility with low-temperature processing. Although surface modification of SnO2 has yielded noteworthy enhancements in device performance over recent years, there remains considerable untapped potential to further refine its efficiency and long-term stability. In this study, THIOACETAMIDE was employed to modify the SnO2 surface, aiming to elevate the quality of the electron transport layer and establish a robust interface with perovskite. The findings underscored that the THIOACETAMIDE-modified SnO2 layer exhibited augmented perovskite absorption in the visible spectrum compared to the control sample. Additionally, the attenuation in photoluminescence intensity within the modified sample alludes to improved electron extraction and enhanced charge transport from the perovskite layer to the electron transport layer. Assessment of solar cell performance unveiled superior and more consistent photovoltaic parameters in the modified sample. Ultimately, the best efficiency was achieved with the perovskite solar cell using SnO2 modified with THIOACETAMIDE, boasting an efficiency of 15.15%

Background: The current treatments of liver diseases are not sufficiently effective, and there has been no therapy that can successfully prevent liver failure and its complications. Previous studies have suggested that resveratrol could inhibit the progression of hepatic diseases based on its antioxidative and anti-inflammatory potentials. Objectives: The present study evaluated the hepato-protective effects of resveratrol in THIOACETAMIDE (TAA)-induced acute liverdamage in rats using neurobehavioral and biochemical parameters. Methods: Forty-eight healthy adult Wistar rats were divided into four groups: C1: healthy control group, C2: non-treated liver failure, E1: liver failure treated with resveratrol 5 mg/kg/day, and E2: liver failure treated with resveratrol 10 mg/kg/day. Aspartate aminotransferase/ alanine aminotransferase (AST/ALT), alkaline phosphatase (Alk), total bilirubin (TB), and plasma-ammonia (NH4) were analyzed, and histopathological evaluations of the specimens were carried out after sacrificing the models. Hepatic encephalopathy (HE) grading, open-field, elevated plus arms, and forced-swimming tests were performed in the study. Results: The resveratrol-treated groups had lower serum concentrations of NH4, ALT, and AST than the C2 group (P < 0. 05). The pathological evaluations demonstrated that resveratrol-treated groups had better outcomes in inflammatory cell infiltration, apoptosis, vacuolization, liver tissue necrosis, and liver damage stage than the C2 group (P < 0. 05). They also showed lower grades of HE, higher locomotor activity (open-field test), and diminished levels of depression (forced-swimming)whencompared to the C2 group (P < 0. 05). Conclusions: Resveratrol supplementation can improve liver damage as AST, ALT, NH4, and tissue damages were decreased after administering the agent in TAA-induced liver damage. Resveratrol can also improve the neurobehavioral manifestations in animal models of liver failure.

Background and Objective: Kombucha (fungal) tea is a sugar sweetened black tea obtained through a fermentation process containing symbiotic culture of acetic acid bacteria and yeasts. This study was done to determine the effect of Kombucha tea on rat liver histophatological alterations due to THIOACETAMIDE (TAA).Materials and Methods: In this experimental study, 20 adult male Wistar rats randomly allocated into four groups as follow: 1) control, 2) TAA group, treated with (TAA), (400 mg/kg/bw) for two weeks, 3) treated with (TAA), (400 mg/kg/bw) and then with Kombucha tea (50 mg/kg) and finally 4) preventive, treated with Kombucha tea, (50 mg/kg) and then (TAA), (400 mg/kg) for three weeks. The serum level of aminotransferase (AST), Alanine transaminase (ALT), Alkaline phosphatase (ALP), Lactate dehydrogenase (LDH) and total bilirubin were meseared and liver tissue samples were stained by hematoxilin and eosin.Results: Serum level of AST, ALT, ALP, LDH and total bilirubin significantly increased in TAA group compare to control group (P<0.05). Serum level of AST, ALT, ALP, LDH and total bilirubin significantly reduced in treated and protective groups in comparision with TAA group (P<0.05). Mitosis and apptosis increased in TAA group. These liver histopathological alterations reduced in terated and protective groups.Conclusion: Kombucha tea contains theraputic and protective effects on enzyms and liver histophatological damage due to THIOACETAMIDE in rat.

Background and Aim: The metabolism of many drugs and toxins is done in the liver and active metabolites are created during the metabolism of these substances which many of them cause liver toxicity. Therefore, the aim of the present study was to investigate the effect of curcumin on liver toxicity induced by THIOACETAMIDE in adult male rats. Materials and Methods: In this experimental study, 48mature female rats were divided into 6 groups including control, sham and 4 experimental groups receiving THIOACETAMIDE (50mg/kg), THIOACETAMIDE plus curcumin30 and 120, 60 mg/kg. In this study, THIOACETAMIDE and curcumin were administered as intraperitoneally in 21 consecutive days. At the end, the activity of enzymes such as alanine aminotransferase, aspartate aminotransferase, alkaline phosphatase, and were measured and liver structure of the animals was investigated. The results were analyzed by ANOVA and Duncan tests at a significant level of p≤ 0. 05. Results: The results of this study showed that THIOACETAMIDE significantly increased the activity of aspartate aminotransferase, alanine aminotransferase and alkaline phosphatase enzymes at the level of p≤ 0. 05 compared to the control group and increased the lymphocyte invasion around the portal of the triad and tissue degradation of the liver. However, curcumin in different doses significantly reduced the activity of these enzymes and improved the liver tissue structure at the level of p≤ 0. 05 compared to the group receiving THIOACETAMIDE. Conclusion: The results of this study showed that THIOACETAMIDE may increase the activity of transaminases and damage the liver tissue structure by producing oxidative stress, while the use of curcumin with THIOACETAMIDE simultaneously probably reduces the activity of transaminases and improves tissue structure due to the antioxidant properties of curcumin.

Background: Cancer occurs in 83% of liver diseases. Other risk factors for liver cancer include viral hepatitis, alcohol consumption, industrial chemicals, and a number of toxins. Another major disease that occurs following liver damage is hepatic encephalopathy. This condition arises primarily due to increased blood ammonia levels. Carvacrol, with antioxidant properties, reduces oxidative stress on the liver. The aim of this study was to investigate the effect of carvacrol on the improvement of hepatic encephalopathy in rats. Methods: In this experimental study, 60 male Wistar rats were randomly divided into six groups of 10 each. Liver damage and induction of oxidative stress were caused in the rats by administering THIOACETAMIDE (100 mg/kg/day) intraperitoneally for three consecutive days. Carvacrol was administered by gavage at 25, 50, or 100 mg/kg/day after THIOACETAMIDE treatment. We investigated the biomarkers of liver damage in the blood, such as alanine transaminase, lactate dehydrogenase, total protein, and bilirubin. We also assessed the effect of oxidative stress, as the key inducer of hepatic encephalopathy, on the liver by measuring the lipid peroxidation, antioxidants, reactive oxygen species, glutathione reserves, and ammonium levels in the serum and brain. Results: THIOACETAMIDE significantly increased the biochemical markers in the rat sera, reflecting ammonium release and the development of oxidative stress (P<0.05). Conversely, the various doses of carvacrol significantly reduced the levels of biomarkers that are indicative of liver damage (P<0.05). Conclusion: The study findings provided experimental evidence in favor of the therapeutic effects of carvacrol and against liver injury induced by THIOACETAMIDE, leading to encephalopathy.