sodium-dodecyl-sulfate and Chemical-and-Drug-Induced-Liver-Injury

The aim of this study was to prepare buoyant (B) melatonin (MT)-loaded chitosan microcapsules having favourable sustained release characteristics (in simulated gastric fluid (SGF), pH 1.2) in comparison with non-buoyant (NB) chitosan particles. The new buoyant microcapsules were prepared by the ionotropic gelation method using sodium lauryl sulfate (NaLS) for coagulation. The microcapsule characteristics were affected by the initial drug and NaLS concentrations, as well as the presence of sodium dioctyl sulfosuccinate (DOS) or pectin with NaLS in the external phase. In general, spherical microcapsules with 36.90-56.23% encapsulation efficiencies, hollow core and satisfactory release properties were produced. The best sustained release profiles (t(50%): 5h) with near zero-order kinetics were observed with the higher theoretical payload microcapsules prepared with both NaLS and DOS in a 1:2 ratio. In vivo studies were also carried out to exploit the protective effect of the MT-loaded NaLS-DOS microcapsules against aflatoxin B1 (AFB1)-induced toxicity (liver apoptosis) in male rats. The results implied that apoptotic rate was significantly reduced when MT or its microcapsules formulation was co-administered with AFB1. The levels of the oxidative stress indices (malondialdehyde (MDA), a lipid peroxidation product and nitric oxide (NO)) in liver tissues were significantly reduced, while the levels of the hepatic antioxidants (glutathione (GSH) and zinc (Zn), as well as the enzyme activities of glutathione reductase (GR), glutathione peroxidase (GSPx) and glutathione-S-transferase (GST)) which act as antiapoptosis were significantly increased as compared to AFB1 group (without MT). MT microcapsules appeared more effective in reduction of apoptotic rate than free MT as indicated by the decline of caspase-3 activities (an apoptotic marker) and confirmed by histopathology.

Topics: Administration, Oral; Aflatoxin B1; Animals; Antioxidants; Apoptosis; Chemical and Drug Induced Liver Injury; Chitin; Chitosan; Delayed-Action Preparations; Dioctyl Sulfosuccinic Acid; Drug Carriers; Free Radical Scavengers; Kinetics; Liver; Male; Melatonin; Microspheres; Oxidative Stress; Pectins; Rats; Rats, Sprague-Dawley; Sodium Dodecyl Sulfate; Surface Properties; Surface-Active Agents; Water; Zinc

Topics: Biopsy; Chemical and Drug Induced Liver Injury; Chemical Phenomena; Chemistry; Complement System Proteins; Cross Reactions; Erythromycin; Hepatitis; Humans; Immunity; Immunity, Cellular; Immunoglobulin A; Immunoglobulin G; Immunoglobulin M; Liver; Lymphocyte Activation; Propionates; Rheumatic Heart Disease; Sodium Dodecyl Sulfate; Stearic Acids; Succinates; Thymidine; Tritium

Topics: Alanine Transaminase; Animals; Aspartate Aminotransferases; Cell Membrane; Chemical and Drug Induced Liver Injury; Environmental Pollution; Fatty Acids, Nonesterified; Fatty Alcohols; Injections, Intraperitoneal; Male; Oxidoreductases; Rats; Sodium Dodecyl Sulfate; Sorbitol; Statistics as Topic; Surface-Active Agents; Time Factors

Topics: Adolescent; Chemical and Drug Induced Liver Injury; Chloramphenicol; Drug Therapy; Erythromycin; Hepatitis; Hepatitis A; Iatrogenic Disease; Nephritis; Sodium Dodecyl Sulfate; Toxicology

Topics: Alkaline Phosphatase; Bilirubin; Chemical and Drug Induced Liver Injury; Clinical Enzyme Tests; Drug Hypersensitivity; Erythromycin; Erythromycin Estolate; Hepatitis A; Jaundice; Liver Diseases; Liver Function Tests; Sodium Dodecyl Sulfate; Toxicology; Transaminases

Topics: Chemical and Drug Induced Liver Injury; Erythromycin; Hepatitis; Humans; Liver; Sodium Dodecyl Sulfate