vitamin-b-12 and Chemical-and-Drug-Induced-Liver-Injury

The possible molecular mechanisms potentially inducing occupational disease among operating room personnel were examined; and the really dangerous anaesthetic agents were identified. As concerns the molecular mechanisms of parenchymatous injury, we surveyed: those connected with free radicals and biological reactive intermediates produced during halothane and nitrous oxide biotransformation; those coming from inorganic fluoride produced during biotransformation of any halogenated anaesthetic agent, and from inorganic bromide released during halothane metabolism; and, finally, those linked to vitamin B12 inactivation from nitrous oxide. Halothane and nitrous oxide can be considered as really dangerous anaesthetic agents for operating room personnel, and enflurane as an agent with marginal toxic power. On the contrary, isoflurane is a safe, useful compound, totally devoided of viscerotoxic effects. From data examined it is possible to conclude that an isoflurane-oxygen-air anaesthesia is safe for operating room personnel more than a balanced anaesthesia with intravenous drugs and nitrous oxide as maintenance.

Topics: Air Pollutants, Occupational; Biodegradation, Environmental; Bromides; Chemical and Drug Induced Liver Injury; Fluorides; Free Radicals; Halothane; Humans; Kidney Diseases; Nervous System Diseases; Nitrous Oxide; Occupational Diseases; Vitamin B 12

Topics: Age Factors; Animals; Blood Coagulation; Cerebrovascular Disorders; Chemical and Drug Induced Liver Injury; Contraceptives, Oral; Contraceptives, Oral, Hormonal; Coronary Disease; Folic Acid; Humans; Hypertension; Metabolism; Myocardial Infarction; Neoplasms; Progestins; Skin; Smoking; Teratogens; Thromboembolism; Time Factors; Vitamin B 12

Ultraviolet C (UVC) devices are an effective means of disinfecting surfaces and protecting medical tools against various microbes, including coronavirus. Overexposure to UVC can induce oxidative stress, damage the genetic material, and harm biological systems. This study investigated the prophylactic efficacy of vitamin C and B12 against hepatotoxicity in UVC-intoxicated rats. Rats were irradiated with UVC (725.76, 967.68, and 1048.36 J/cm

Topics: Animals; Antioxidants; Ascorbic Acid; Chemical and Drug Induced Liver Injury; Liver; Male; Oxidative Stress; Rats; Vitamin A; Vitamin B 12; Vitamins

Acetaminophen is a pharmaceutical synthesized non-opioid analgesic that belongs to the "aniline analgesics" class of medicine. Because it lacks a significant anti-inflammatory effect, it is not classified as a non-steroidal anti-inflammatory therapeutic medication (NSAID). As an over-the-counter pain reliever and antipyretic, Acetaminophen is the active metabolite of phenacetin and acetanilide, but it is less toxic than either precursor. According to some medical studies, Acetaminophen toxicity can be treated with vitamin B12. Acetaminophen-poisoned Male Wister rats were the subject model of the current study, which examines the effects of vitamin B12 on their hepatic health. There were three groups of animals: Acetaminophen treated animals (750 ml/kg), vitamin B12-treated animals (0.63 g/kg), and a control group that received distilled water (750 ml/kg). All animals were given oral medication for seven days. On the seventh day, the animal was sacrificed. Plasma levels of Alanine aminotransferase (ALT), Aspartate aminotransferase (AST), Glutathione (GSH), total antioxidant capacity (TAC), Caspase3, Malondialdehyde (MDA), Interleukin-6 (IL-6), and tumor necrosis factor-alpha (TNF-) were measured in the cardiac blood samples. Vitamin B12 lowers liver enzyme levels in the blood, increases overall antioxidant levels, and compensates for tissue glutathione deficiency while lowering serum elevations. TNF-α and interleukin-6 levels are also reduced by caspase3. Acetaminophen-induced hepatic necrosis and inflammatory cell infiltration were both considerably reduced by vitamin B12 supplementation. According to this study, vitamin B12 was found to have a protective effect against acetaminophen-induced hepatotoxicity.

Topics: Acetaminophen; Animals; Anti-Inflammatory Agents; Antioxidants; Chemical and Drug Induced Liver Injury; Interleukin-6; Male; Rats; Rats, Wistar; Rodent Diseases; Vitamin B 12

Potassium bromate (PB) is a food enhancer, water disinfection by-product, and a proven carcinogen. It elicits toxicities in the living organism due to exposure and in a dose-dependent manner. The present study discourses the ameliorative efficacy of riboflavin (RF) in PB-administered rodents. The animals were distributed into five treatment groups: control (group I), PB alone (group II, 150 mg/kg), RF alone (group III, 2 mg/kg), PB+RF1 (group IV, 150 mg/kg + 2 mg/kg), and PB+RF2 (group V, 150 mg/kg + 4 mg/kg). After the round of the treatment, the animals were sacrificed to collect their blood and liver samples for the detailed analysis. Group II depicted perturbed liver functions evidenced by altered serum and toxicity markers along with the disturbed redox balance. Also, these biochemical results were found harmonious with histopathological analysis and comet assay. However, group III showed no noticeable alteration in the same parameters, whereas the combination groups (IV and V) exhibited dose-dependent amelioration in the PB-induced toxicities. Interestingly, RF favored apoptosis concomitant with suppressing the necrosis in the PB-challenged groups, as shown by the activity of caspase-3 and lactate dehydrogenase. Histopathological analysis and comet assay further consolidate these results. Hence, RF has significant alleviative property against PB-induced hepatotoxicity in vivo that can be used in the consumer items containing the toxicant.

Topics: Animals; Apoptosis; Bromates; Caspase 3; Chemical and Drug Induced Liver Injury; L-Lactate Dehydrogenase; Liver; Male; Rats; Vitamin B 12

In the study, we aimed to show the effects of vitamin B12 on the necrosis caused by methotrexate (MTX), a folic acid antagonist. Thirty-two rats were randomly assigned to four groups of eight rats per group. Control (n = 8), Vit B12 (n = 8) 3 μg/kg/ip B12 (15 days) per day throughout the experiment, MTX (n = 8) injected with a single dose of 20 mg/kg/ip MTX on 8th day of experiment, MTX + Vit B12 (n = 8) injected with a single dose of 20 mg/kg ip methotrexate on 8th day of experiment + 3 μg/kg/ip Vit B12 (15 days) per day throughout the experiment. Oxidant (TOS)/antioxidant (TAS) system, TNF-α and TGF-β levels, AST and ALT, serum vitamin B12 levels were determined in the tissue. Cyclooxygenase-2 (Cox-2), receptor-interacting protein kinase 1 (RIP1) and 3 (RIP3) immunohistochemistry were applied to the liver tissue. TOS increased; TAS decreased; TNF-α and TGF-β levels increased; AST and ALT levels changed after MTX hepatotoxicity. Vit B12 decreased significantly. COX-2, RIP1, and RIP3 immunoreactivity increased. Vit B12 showed improvement in all of the negative results. Vit B12 is an important supplement to be used against necrosis in tissue after MTX hepatotoxicity.

Topics: Animals; Antimetabolites, Antineoplastic; Chemical and Drug Induced Liver Injury; Male; Methotrexate; Rats; Rats, Wistar; Receptor-Interacting Protein Serine-Threonine Kinases; Treatment Outcome; Vitamin B 12

Several vitamins, including C, E, and B. An in vitro model of freshly isolated rat hepatocytes was utilized for assessing hepatocyte mitochondrial activity conducted by cell proliferation assay (MTT). The isolated hepatocytes were treated with vitamin C, vitamin E, vitamin B. In vitro results showed that vitamins C and B and the combination preparation significantly increased the percentage of hepatocyte mitochondrial activity, both with and without the addition of APAP (. Pretreatment with vitamins C, E, B

Topics: Acetaminophen; Animals; Antioxidants; Ascorbic Acid; Chemical and Drug Induced Liver Injury; Liver; Male; Oxidative Stress; Rats; Rats, Sprague-Dawley; Vitamin B 12; Vitamin E

Isoniazid (INH) and Rifampicin (RIF) are known hepatotoxic agents. We compared the efficacy of Spirulina fusiformis and its active components vitamin B12 and beta-carotene in attenuating INH and RIF induced hepatotoxicity. We also tried to elucidate the inflammatory mechanism behind anti-tuberculosis drug induced hepatotoxicity. INH and RIF were administered to Wistar albino rats for 28 days to induce hepatotoxicity. S. fusiformis, vitamin B12, and beta-carotene were co-administered with INH and RIF and their hepatoprotective, antioxidant, and immunomodulatory roles were studied through blood and liver analysis. Changes induced by INH and RIF in antioxidants, cytokines (IL-6 and IL-10) and expression of Nuclear Factor-κB (NF-κB) and Nitric Oxide Synthase (iNOS) were also studied. Supplement treatment caused restoration of liver function parameters to normal levels along with reversal of inflammatory changes in IL-6 and IL-10 levels. Liver PCNA, iNOS, and NF-κB expression were reduced in the supplement treated tissues compared to INH and RIF treated rats as evidenced by immunohistochemistry and quantitative PCR. Correlation of IL-6 levels, PCNA, and iNOS with NF-κB showed its pivotal role in the inflammatory process. Study shows the pivotal role of NF-kB and the equivalence in antioxidant efficacy of vitamin B12 and beta-carotene compared to Spirulina fusiformis. J. Cell. Biochem. 118: 3825-3833, 2017. © 2017 Wiley Periodicals, Inc.

Topics: Animals; Antitubercular Agents; beta Carotene; Chemical and Drug Induced Liver Injury; Dietary Supplements; Female; Interleukin-10; Interleukin-6; Liver; NF-kappa B; Nitric Oxide Synthase Type II; Oxidative Stress; Rats; Rats, Wistar; Spirulina; Vitamin B 12

The present study elucidated the protective role of vitamin B(12) with folic acid against arsenic-induced hepatotoxicity in female rats. Ingestion of sodium-arsenite- contaminated water [0.4 ppm/100 g body weight (b.w.)/day] in combination with vitamin B(12) plus folic acid (0.07 and 4.0 μg, respectively/100 g b.w./day) for 24 days to Wistar rats offered a significant protection against alone arsenic-induced distorted liver function, damaged histoarchitecture, elevated oxidative stress, and DNA fragmentation of hepatic tissues. Arsenic only exposure decreased hepatic superoxide dismutase (SOD), catalase activities, and the level of nonprotein-soluble thiol (NPSH), with a concomitant increase in thiobarbituric acid reactive substances (TBARS) and conjugated dienes (CDs) in the liver. Vitamin supplementation restrained the increase of TBARS and CDs by restoring catalase, SOD, and NPSH levels. Restricted generation of free radicals may be correlated to the protection of DNA stability and hepatic morphology. This study explains the decisive role of vitamin B(12) with folic acid to ameliorate arsenic-mediated liver injuries.

Topics: Animals; Arsenites; Chemical and Drug Induced Liver Injury; DNA Fragmentation; Drug Therapy, Combination; Female; Folic Acid; Liver; Liver Function Tests; Oxidative Stress; Rats; Rats, Wistar; Sodium Compounds; Thiobarbituric Acid Reactive Substances; Vitamin B 12; Vitamin B Complex

Topics: Chemical and Drug Induced Liver Injury; Ethanol; Humans; Liver; Protective Agents; Psychotropic Drugs; S-Adenosylmethionine; Substance-Related Disorders; Vitamin B 12; Vitamin B Complex

Vitamin B(12) contains a cobalt complex and accumulates at high levels in the liver. Vitamin B(12) was examined for its hepatoprotective effect on dimethylnitrosamine-induced liver injury in mice. Vitamin B(12) decreased the blood levels of aspartate aminotransferase and alanine aminotransferase, and clearly inhibited the overaccumulation of collagen fibrils. Reverse transcription-polymerase chain reaction (RT-PCR) analysis of the liver showed that the gene expression of alpha-smooth muscle actin and heat-shock protein 47, which are markers of fibrosis, were suppressed by vitamin B(12) administration. Our findings indicate that vitamin B(12) could be an effective hepatoprotective agent.

Topics: Alanine Transaminase; Alkylating Agents; Animals; Aspartate Aminotransferases; Chemical and Drug Induced Liver Injury; Dimethylnitrosamine; Liver Cirrhosis; Liver Cirrhosis, Experimental; Liver Function Tests; Mice; Mice, Inbred BALB C; Reverse Transcriptase Polymerase Chain Reaction; Vitamin B 12; Vitamins

Topics: Acetaminophen; Adult; Azulenes; Bis-Trimethylammonium Compounds; Chemical and Drug Induced Liver Injury; Cysteine; Drug Combinations; Female; Humans; Inositol; Liver; Liver Extracts; Sesquiterpenes; Vitamin B 12

A comparative study of the hepatoprotective effect of carnosine and 4-methyluracil under CCl4-induced acute toxic hepatitis has been carried out. The extent of liver injury and its regeneration were established from morphological data as well as from changes in the activities of alanine aminotransferase (ALT) and histidase and the bilirubin content in blood serum. Hyperlipoperoxidation in the liver and serum was assessed by the amount of TBA-active products. It was found that by day 10 of experimental hepatitis ALT and histidase levels in blood sera of untreated animals exceeded the normal values 1.3- and 3.9-fold, whereas those in the carnosine-treated group approximated the values characteristic of intact animals. The activity of serum ALT in animals treated with vitamin B12 or 4-methyluracil exceeded normal values 1.5 and 1.6 times, whereas that of histidase was 2.5 and 2.7 times as high. Carnosine and 4-methyluracil inhibited (in approximately the same degree) the formation of TBA-active products in the liver. According to morphological dta, cessation of CCl4 injections was accompanied by rapid regeneration of liver tissues in all animal groups. Carnosine enhanced regenerative processes in parenchymatous and connective tissues in a far greater degree in comparison with other drugs. The mitotic index in the carnosine-treated group exceeded more than twofold the corresponding parameters in untreated animals. Possible mechanisms of carnosine action on liver repair are discussed.

Topics: Alanine Transaminase; Animals; Carbon Tetrachloride Poisoning; Carnosine; Chemical and Drug Induced Liver Injury; Histidine Ammonia-Lyase; Lipid Peroxidation; Liver; Male; Rats; Thiobarbiturates; Uracil; Vitamin B 12

Topics: Antipsychotic Agents; Butyrophenones; Chemical and Drug Induced Liver Injury; Drug Therapy, Combination; Female; Humans; Liver Diseases; Liver Extracts; Male; Mental Disorders; Phenothiazines; Uridine Diphosphate Glucose; Uridine Diphosphate Sugars; Vitamin B 12

Topics: Adenosine Monophosphate; Alcohol Withdrawal Delirium; Alcoholism; Chemical and Drug Induced Liver Injury; Chlormethiazole; Deanol; Drug Combinations; Humans; Methionine; Psychoses, Alcoholic; Vitamin B 12

Topics: Anabolic Agents; Blood Cell Count; Blood Transfusion; Bone Marrow; Bone Marrow Diseases; Bone Marrow Examination; Bone Marrow Transplantation; Chemical and Drug Induced Liver Injury; Child, Preschool; Chloramphenicol; Female; Folic Acid; Hematopoiesis; Humans; Kidney Diseases; Methenolone; Penicillin G; Prednisolone; Vitamin B 12

Topics: Animals; Ascorbic Acid; Biotin; Carbon Tetrachloride Poisoning; Centrifugation; Chemical and Drug Induced Liver Injury; Folic Acid; Liver; Necrosis; Nicotinic Acids; Pantothenic Acid; Proteins; Pyridoxine; Rats; Riboflavin; Specimen Handling; Thiamine; Vitamin A; Vitamin B 12; Vitamin E; Vitamins

Topics: Animals; Carbon Tetrachloride Poisoning; Chemical and Drug Induced Liver Injury; Cortisone; Lipid Metabolism; Liver; Liver Glycogen; Male; Phosphoric Monoester Hydrolases; Rats; RNA; Vitamin B 12

Topics: Adult; Aged; Arginine; Chemical and Drug Induced Liver Injury; Citrulline; Female; Folic Acid; Humans; Male; Middle Aged; Niacinamide; Ornithine; Vitamin B 12

Topics: Animals; Aspartate Aminotransferases; Chemical and Drug Induced Liver Injury; Dogs; Rats; Vitamin B 12

Topics: Biliary Tract Diseases; Chemical and Drug Induced Liver Injury; Chronic Disease; Fatty Liver; Health Resorts; Hepatitis; Humans; Liver Cirrhosis; Liver Diseases; Vitamin B 12

Topics: Carbon Tetrachloride Poisoning; Chemical and Drug Induced Liver Injury; Hepatitis; Rats; Toxicology; Vitamin B 12; Vitamin B Complex

Topics: Animals; Blood Proteins; Carbon Tetrachloride Poisoning; Chemical and Drug Induced Liver Injury; In Vitro Techniques; Liver; Rats; Vitamin B 12

Topics: Amino Acids; Aspartic Acid; Carbon Tetrachloride Poisoning; Chemical and Drug Induced Liver Injury; Hepatitis; Liver Extracts; Magnesium; Pharmacology; Potassium; Purines; Rats; Research; Toxicology; Vitamin B 12; Vitamin B Complex; Yeast, Dried

Topics: Bile; Carbon Tetrachloride Poisoning; Chemical and Drug Induced Liver Injury; Fatty Liver; Hepatitis; Lipid Metabolism; Liver Glycogen; Metabolism; Pharmacology; Rats; Research; Toxicology; Vitamin B 12

Topics: Carbon Tetrachloride Poisoning; Chemical and Drug Induced Liver Injury; Folic Acid; Hepatitis; Leucovorin; Liver; Metabolism; Niacin; Nicotinic Acids; Pantothenic Acid; Pyridoxine; Rats; Research; Thiamine; Toxicology; Vitamin B 12; Vitamin B Complex; Vitamins

Topics: Blood; Chemical and Drug Induced Liver Injury; Chlorpromazine; Cholangitis; Diagnosis; Hepatitis; Hepatitis A; Humans; Jaundice; Jaundice, Obstructive; Liver Cirrhosis; Liver Diseases; Liver Neoplasms; Monoamine Oxidase Inhibitors; Prognosis; Vitamin B 12

Topics: Avitaminosis; Carbon Tetrachloride Poisoning; Chemical and Drug Induced Liver Injury; DNA; Folic Acid; Folic Acid Deficiency; Hepatitis; Liver Diseases; Liver Regeneration; Metabolism; Necrosis; Pharmacology; Rats; Research; Thymidine; Uracil; Vitamin B 12

Topics: Chemical and Drug Induced Liver Injury; Cobalt Isotopes; Hepatitis; Hepatitis A; Humans; Jaundice; Jaundice, Obstructive; Liver Diseases; Liver Function Tests; Toxicology; Vitamin B 12

Topics: Chemical and Drug Induced Liver Injury; Cobamides; Coenzymes; Corrinoids; Hematinics; Hepatitis; Hepatitis A; Vitamin B 12

Topics: Animals; Carbon Tetrachloride Poisoning; Chemical and Drug Induced Liver Injury; Corrinoids; Hepatitis; Hepatitis A; Hormones; Liver Function Tests; Pineal Gland; Rats; Research; Sulfobromophthalein; Vitamin B 12

Topics: Carbon Tetrachloride Poisoning; Chemical and Drug Induced Liver Injury; Dogs; Glucuronates; Hepatitis; Hormones; Liver; Metabolism; Pharmacology; Pineal Gland; Research; Vitamin B 12; Vitamin B Complex

Topics: Animals; Carbon Tetrachloride Poisoning; Chemical and Drug Induced Liver Injury; Hepatitis; Hepatitis A; Iodine Isotopes; Liver Diseases; Liver Function Tests; Vitamin B 12

Topics: Chemical and Drug Induced Liver Injury; Cytochromes; Electron Transport Complex II; Fructose-Bisphosphate Aldolase; Hepatitis; Liver; Succinate Dehydrogenase; Vitamin B 12

Topics: Chemical and Drug Induced Liver Injury; Corrinoids; Cytochromes; Hepatitis; Hepatitis, Chronic; Prednisolone; Vitamin B 12