ABSTRACT
The effect of thymoquinone (TQ), the main constituent of the volatile oil of black seed (Nigella sativa), on the guinea-pig isolated tracheal zig-zag preparation was investigated. TQ caused a concentration-dependent decrease in the tension of the tracheal smooth muscle precontracted by carbachol. The effects of TQ were significantly potentiated by pretreatment of the tracheal preparations with quinacrine, a phospholipase A2 inhibitor, nordihydroguiaretic acid, a lipoxygenase inhibitor and by pretreatment with methylene blue, an inhibitor of soluble guanylyl cyclase. On the other hand, the effects of TQ were not influenced by pretreatment of the tracheal preparations with indomethacin, a cyclooxygenase inhibitor, propranolol, a non-selective beta-adrenoceptor blocker or by the pretreatment with theophylline, an adenosine receptors antagonist TQ totally abolished the pressor effects of histamine and serotonin on the guinea-pig isolated tracheal and ileum smooth muscles. The results of the present study suggest that TQ induced relaxation of precontracted tracheal preparation is probably mediated, at least in part, by inhibition of lipoxygenase products of arachidonic acid metabolism and possibly by non-selective blocking of the histamine and serotonin receptors. This relaxant effect of TQ, further support the traditional use of black seeds either alone or in combination with honey to treat bronchial asthma.
Subject(s)
Benzoquinones/pharmacology , Muscle Relaxation/drug effects , Animals , Carbachol/antagonists & inhibitors , Carbachol/pharmacology , Dose-Response Relationship, Drug , Guinea Pigs , Male , Muscle Contraction/drug effects , Trachea/drug effectsABSTRACT
Light-dependent H2 evolution did not occur in nitrogen-deprived cultures of Rhodovulum sulfidophilum in the presence of ethanol. When ethanol was added to cells which had been grown with ammonia, derepression of the nitrogen fixation genes (nifHD) was inhibited at an ethanol concentration of 1 mM. On the other hand, when cells had nitrogenase-catalyzed proton-reducing activity prior to ethanol addition, reduction of the nifHD transcript level did not occur after the addition. In cells grown with ammonia, concomitant addition of an auxiliary oxidant such as dimethylsulfoxide or sodium bicarbonate resulted in derepression of nitrogenase activity in the presence of ethanol. These results suggest that the electron-accepting process is necessary for derepression of nif genes in cultures which use ethanol as the electron donor.
Subject(s)
Anti-Infective Agents, Local/pharmacology , Ethanol/pharmacology , Nitrogen/pharmacology , Nitrogenase/metabolism , Rhodobacter/drug effects , Rhodobacter/enzymology , Ammonia/pharmacology , Anti-Infective Agents, Local/metabolism , Dimethyl Sulfoxide/pharmacology , Ethanol/metabolism , Free Radical Scavengers/pharmacology , Gene Expression Regulation, Bacterial/drug effects , Gene Expression Regulation, Enzymologic/drug effects , Genes, Bacterial/drug effects , Nitrogen Fixation/drug effects , Nitrogen Fixation/genetics , Photosynthesis/physiology , Sodium Bicarbonate/pharmacologyABSTRACT
Thymoquinone, the active constituent of Nigella sativa, was tested in isolated rat hepatocytes as a hepatoprotective agent against tert-butyl hydroperoxide (TBHP) toxicity. TBHP (2 mM) was used to produce oxidative injury in isolated rat hepatocytes and caused progressive depletion of intracellular glutathione (GSH), loss of cell viability as evidenced by trypan blue uptake and leakage of cytosolic enzymes, alanine transaminase (ALT) and aspartic transaminase (AST). Preincubation of hepatocytes with 1 mM of either thymoquinone or silybin, which is a known hepatoprotective agent, resulted in the protection of isolated hepatocytes against TBHP induced toxicity evidenced by decreased leakage of ALT and AST, and by decreased trypan blue uptake in comparison to TBHP treated hepatocytes. Both thymoquinone and silybin prevented TBHP induced depletion of GSH to the same extent. Although thymoquinone protected the liver enzymes leakage, the degree of protection was less than that caused by silybin.