ABSTRACT
Keratinocytes, the major cell type of the epidermis, are particularly sensitive to environmental factors including exposure to sunlight and chemical agents. Since oxidative stress may arise as a result of these factors, compounds are actively sought that can act as protective agents. Recently, cannabidiol (CBD), a phytocannabinoid found in Cannabis Sativa L., has gained increased interest due to its anti-inflammatory and antioxidant properties, and absence of psychoactive effects. This prompted us to analyze the protective effects of CBD on keratinocytes exposed to UVB irradiation and hydrogen peroxide. Here we show, using liquid chromatography mass spectrometry, that CBD was able to penetrate keratinocytes, and accumulated within the cellular membrane. CBD reduced redox balance shift, towards oxidative stress, caused by exposure UVB/hydrogen peroxide, estimated by superoxide anion radical generation and total antioxidant status and consequently lipid peroxidation level. CBD was found to protect keratinocytes by preventing changes in the composition of the cellular membrane, associated with UVB/hydrogen peroxide damages which included reduced polyunsaturated fatty acid levels, increased sialic acid and lipid peroxidation products (malondialdehyde and 8-isoprostanes) levels. This maintains cell membranes integrity and prevents the release of lactate dehydrogenase. In addition, CBD prevented UVB/hydrogen peroxide-induced reduction of keratinocyte size and zeta potential, and also decreased activity of ATP-binding cassette membrane transporters. Together, these findings suggest that CBD could be a potential protective agent for keratinocytes against the harmful effects of irradiation and chemical environmental factors that cause oxidative stress.
Subject(s)
Cannabidiol , Hydrogen Peroxide , Antioxidants/pharmacology , Cannabidiol/pharmacology , Cell Membrane , Keratinocytes , Oxidative Stress , Ultraviolet Rays/adverse effectsABSTRACT
Ethanol is oxidized to acetaldehyde and then to acetic acid and these processes are accompanied by free radical generation. This paper reports the effect of green tea on electric charge and phospholipids composition of erythrocytes membrane from rats intoxicated with ethanol. Electrophoresis technique and HPLC have been applied to above-mentioned studies. Ethanol administration caused increase in erythrocyte membrane surface charge density and phospholipid composition. Ingestion of green tea with ethanol partially prevented changes in structure and function of membrane caused by chronic ethanol intoxication.
Subject(s)
Alcoholism/metabolism , Erythrocyte Membrane/drug effects , Phospholipids/metabolism , Plant Extracts/pharmacology , Tea/chemistry , Animals , Electrophoresis , Erythrocyte Membrane/chemistry , Erythrocyte Membrane/metabolism , Ethanol/pharmacology , Hydrogen-Ion Concentration , Isoelectric Point , Lipid Peroxidation/drug effects , Male , Phospholipids/analysis , Rats , Rats, Wistar , Static ElectricityABSTRACT
Methanol is oxidized in-vivo to formaldehyde and then to formate, and these processes are accompanied by the generation of free radicals. We have studied the effect of N-acetylcysteine on liver cell membrane from rats intoxicated with methanol (3.0 g kg(-1)). Evaluation of the effect was achieved by several methods. Lipid peroxidation and surface charge density were measured. An ultrastructural study of the liver cells was undertaken. The concentration of marker enzymes of liver damage (alanine aminotransferase and aspartate aminotransferase) in blood serum was measured. Methanol administration caused an increase in lipid peroxidation products (approximately 30%) as well as in surface charge density (approximately 60%). This might have resulted in the membrane liver cell damage visible under electron microscopy and a leak of alanine aminotransferase and aspartate aminotransferase into the blood (increase of approximately 70 and 50%, respectively). Ingestion of N-acetylcysteine with methanol partially prevented these methanol-induced changes. Compared with the control group, lipid peroxidation was increased by approximately 3% and surface charge density by approximately 30%. Alanine aminotransferase and aspartate aminotransferase activity increased by 9 and 8%, respectively, compared with the control group. The results suggested that N-acetylcysteine was an effective antioxidant in methanol intoxication. It may have efficacy in protecting free radical damage to liver cells following methanol intoxication.
Subject(s)
Acetylcysteine/pharmacology , Free Radical Scavengers/pharmacology , Liver/drug effects , Methanol/pharmacology , Solvents/pharmacology , Alanine Transaminase/blood , Alanine Transaminase/drug effects , Animals , Aspartate Aminotransferases/blood , Aspartate Aminotransferases/drug effects , Cell Membrane/drug effects , Cell Membrane/metabolism , Lipid Peroxidation/drug effects , Lipid Peroxidation/physiology , Liver/cytology , Liver/metabolism , Male , Methanol/metabolism , Rats , Rats, Wistar , Solvents/metabolismABSTRACT
Methanol is oxidized in vivo to formaldehyde and then to formate and these processes are accompanied by free radicals generation. This paper reports the effect of antioxidants: trolox derivative (U-83836E) and N-acetylcysteine (NAC) on lipid peroxidation, surface charge density and hematological parameters of erythrocytes from rats intoxicated with methanol (3.0 g/kg body weight). Methanol administration caused increase in erythrocyte lipid peroxidation products and changes in surface charge density. Ingestion of methanol with U-83836E and NAC partially prevented these methanol-induced changes. This suggests that U83836E and NAC act as effective antioxidants and free radicals scavengers. They may have efficacy in protecting free radical damage to erythrocytes following methanol intoxication.
