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Biotechnology and Applied Biochemistry Jun 2022In this study, the effects of curcumin, glutathione (GSH), malondialdehyde (MDA) levels, advanced protein oxidation products (AOPP), superoxide dismutase (SOD), and...
Examination of the effect of curcumin in experimental liver damage created by diethylnitrosamine in Swiss albino mice to superoxide dismutase and catalase activities and glutathione, malondialdehyde, and advanced oxidation protein products levels.
In this study, the effects of curcumin, glutathione (GSH), malondialdehyde (MDA) levels, advanced protein oxidation products (AOPP), superoxide dismutase (SOD), and catalase (CAT) activities in experimental liver damage with diethylnitrosamine (DEN) in Swiss albino mice were investigated. The subjects (n = 9) used in the study were divided into 5 groups as tumor control 1, tumor control 2, curcumin protective, curcumin treatment and healthy control groups Curcumin oral gavage (in 150 mg/kg of ethylalcohol) was given to the protecting group for 19 days, 5 days before the administration of DEN, and 24 h after the administration of DEN. Hundred microliters of ethylalcohol oral gavage was given to the healthy group for 19 days. While MDA levels decreased significantly in the curcumin preservative group (p < 0.05), (p = 0.002), the decrease was not significant in the treatment groups (p > 0.05), (p = 0.128). AOPP levels decreased significantly in the curcumin protective group (p < 0.05), (p = 0.009) but the decrease in the treatment group was not found significant (p > 0.05), (p = 0.073). SOD activities increased significantly in both groups. It was found as (p < 0.05), (p = 0.001) and (p < 0.05), (p = 0.002), respectively. GSH levels decreased but these reductions were not found statistically significant. CAT activities increased significantly in both groups. It was determined as (p < 0.05), (p = 0.001) for both groups.
Topics: Advanced Oxidation Protein Products; Animals; Antioxidants; Catalase; Curcumin; Diethylnitrosamine; Glutathione; Humans; Liver; Malondialdehyde; Mice; Oxidative Stress; Superoxide Dismutase
PubMed: 34041781
DOI: 10.1002/bab.2198 -
European Journal of Cancer Prevention :... Dec 2004The anticancer efficacy of tocotrienol-rich fraction (TRF) was evaluated during diethylnitrosamine (DEN)/2-acetylaminofluorene (AAF)-induced hepatocarcinogenesis in male...
The anticancer efficacy of tocotrienol-rich fraction (TRF) was evaluated during diethylnitrosamine (DEN)/2-acetylaminofluorene (AAF)-induced hepatocarcinogenesis in male Sprague-Dawley rats. TRF treatment was carried out for 6 months, and was started 2 weeks before initiation phase of hepatocarcinogenesis. Morphological examination of the livers from DEN/AAF rats showed numerous off-white patches and few small nodules, which were significantly reduced by TRF treatment. Cytotoxic damage by DEN/AAF was estimated by alkaline phosphatase (ALP) release into the plasma from the cell membranes. DEN/AAF caused a twofold increase in the activity of ALP in plasma as compared with normal control rats, and this increase was prevented significantly by TRF treatment. We observed an increase of 79% in liver ALP activity in DEN/AAF rats, which was further increased by another 48% after the administration of TRF. Hepatic activity of glutathione S-transferase (GST) was also increased (3.5-fold) during the induction of hepatic carcinogenesis. Lipid peroxidation and low-density lipoprotein (LDL) oxidation increased threefold following initiation by DEN/AAF as compared with normal control rats. However, TRF treatment to DEN/AAF-treated rats substantially decreased (62-66%) the above parameters and thus limited the action of DEN/AAF. We conclude that long-term intake of TRF could reduce cancer risk by preventing hepatic lipid peroxidation and protein oxidation damage due to its antioxidant actions.
Topics: 2-Acetylaminofluorene; Alkylating Agents; Animals; Anticholesteremic Agents; Antioxidants; Carcinogens; Chemoprevention; Diethylnitrosamine; Lipid Peroxidation; Liver Neoplasms; Male; Neoplasms, Experimental; Oxidative Stress; Plant Oils; Proteins; Rats; Rats, Sprague-Dawley; Rice Bran Oil; Tocotrienols
PubMed: 15548946
DOI: 10.1097/00008469-200412000-00009 -
Analytical Chemistry May 2020Diversified oxidized-lipid molecules are responsible for inflammation and cell death, including ferroptosis. Lipid radicals are the source of these oxidized lipids,...
Diversified oxidized-lipid molecules are responsible for inflammation and cell death, including ferroptosis. Lipid radicals are the source of these oxidized lipids, which are the initial key molecules in the lipid peroxidation chain reaction. However, owing to their extremely high reactivity and short half-life, an established detection technique is not available. Here, we propose a high-performance liquid chromatography fluorometry and high-resolution tandem mass spectrometry system combined with a fluorescent probe as a structural analysis method for lipid-derived radicals. We detected 132 lipid-derived radicals, including 111 new species, from five polyunsaturated fatty acids. In addition, a database was constructed for which the initial fatty acid could be determined using the radical structure. Further, 12 endogenous lipid-derived radicals were identified in carcinogen-induced liver cancer mouse models. Therefore, this method and its corresponding database will provide novel insights into mechanisms underlying the lipid peroxidation, including the associated inflammation and ferroptosis.
Topics: Animals; Diethylnitrosamine; Disease Models, Animal; Free Radicals; Injections, Intraperitoneal; Lipids; Liver Neoplasms; Male; Mice; Mice, Inbred C57BL; Molecular Structure
PubMed: 32311262
DOI: 10.1021/acs.analchem.0c00053 -
Report on Carcinogens : Carcinogen... 2002
Topics: Animals; Carcinogens; Diethylnitrosamine; Environmental Exposure; Government Regulation; Humans; United States
PubMed: 15326697
DOI: No ID Found -
Report on Carcinogens : Carcinogen... 2004
Topics: Animals; Carcinogenicity Tests; Carcinogens; Cricetinae; Diethylnitrosamine; Environmental Exposure; Female; Government Regulation; Guidelines as Topic; Humans; Male; Models, Biological; Rats; United States
PubMed: 21089927
DOI: No ID Found -
Report on Carcinogens : Carcinogen... 2002
Topics: Animals; Carcinogens; Diethylnitrosamine; Environmental Exposure; Government Regulation; Humans; United States
PubMed: 15326696
DOI: No ID Found -
Report on Carcinogens : Carcinogen... 2004
Topics: Alkylating Agents; Animals; Animals, Newborn; Birds; Carcinogenicity Tests; Carcinogens; Cricetinae; Diethylnitrosamine; Dogs; Environmental Exposure; Fishes; Gerbillinae; Government Regulation; Guidelines as Topic; Guinea Pigs; Haplorhini; Hedgehogs; Humans; Mesocricetus; Mice; Models, Biological; Rabbits; Rats; United States
PubMed: 21089928
DOI: No ID Found -
Journal of Toxicology. Clinical... Aug 1982A number of amines and quaternary ammonium salts can be nitrosated to N-nitrosamines under environmental conditions as well as in vivo. Of the N-nitrosamines which have... (Review)
Review
A number of amines and quaternary ammonium salts can be nitrosated to N-nitrosamines under environmental conditions as well as in vivo. Of the N-nitrosamines which have been bioassayed to date, more than 250 are proven animal carcinogens. In the absence of data which document that N-nitrosamines can be carcinogenic to man, we concur with the International Agency for Research on Cancer that those nitrosamines that were proven carcinogens in at least 2 animal species "should be regarded for practical purposes as if they were carcinogenic to humans" (1). Such evaluation pertains also to N-nitrosodiethanolamine (NDELA), N-nitrosomorpholine (NMOR) and the tobacco-specific N-nitrosamines (TSNA). This presentation discusses the environmental occurrence, analysis, reduction, bioassay data for carcinogenicity and metabolism of these 3 types of nitrosamines. The data at hand make it prudent to encourage reduction of the occurrence of N-nitrosamines in the workplace, in the environment and in food, tobacco and other personal use products. Emphasis should also be placed on research efforts to inhibit the in vivo formation of N-nitrosamines and their metabolic activation to reactive carcinogenic species. The latter efforts require increased knowledge as to the activation of nitrosamines and their reaction with cellular macromolecules including DNA.
Topics: Animals; Carcinogens, Environmental; Chromatography, Gas; Diethylnitrosamine; Environmental Pollutants; Food Analysis; Humans; Mice; Nitrosamines; Plants, Toxic; Rats; Smoke; Nicotiana
PubMed: 6761448
DOI: 10.3109/15563658208990397 -
International Journal of Biological... Mar 2024Growing evidence confirms associations between glycogen metabolic re-wiring and the development of liver cancer. Previous studies showed that glycogen structure changes...
Growing evidence confirms associations between glycogen metabolic re-wiring and the development of liver cancer. Previous studies showed that glycogen structure changes abnormally in liver diseases such as cystic fibrosis, diabetes, etc. However, few studies focus on glycogen molecular structural characteristics during liver cancer development, which is worthy of further exploration. In this study, a rat model with carcinogenic liver injury induced by diethylnitrosamine (DEN) was successfully constructed, and hepatic glycogen structure was characterized. Compared with glycogen structure in the healthy rat liver, glycogen chain length distribution (CLD) shifts towards a short region. In contrast, glycogen particles were mainly present in small-sized β particles in DEN-damaged carcinogenic rat liver. Comparative transcriptomic analysis revealed significant expression changes of genes and pathways involved in carcinogenic liver injury. A combination of transcriptomic analysis, RT-qPCR, and western blot showed that the two genes, Gsy1 encoding glycogen synthase and Gbe1 encoding glycogen branching enzyme, were significantly altered and might be responsible for the structural abnormality of hepatic glycogen in carcinogenic liver injury. Taken together, this study confirmed that carcinogenic liver injury led to structural abnormality of hepatic glycogen, which provided clues to the future development of novel drug targets for potential therapeutics of carcinogenic liver injury.
Topics: Rats; Animals; Carcinogens; Diethylnitrosamine; Liver Glycogen; Liver; Liver Neoplasms; Glycogen; Carcinogenesis
PubMed: 38228208
DOI: 10.1016/j.ijbiomac.2024.129432 -
Biochemical Pharmacology Jun 1989
Topics: Diethylnitrosamine; Female; Humans; In Vitro Techniques; Male; Microsomes, Liver; Nasal Mucosa; Oxidoreductases; Smoking
PubMed: 2735943
DOI: 10.1016/0006-2952(89)90424-3