Evaluation of in vitro antioxidant activity of Indian bay leaf, Cinnamomum tamala (Buch. -Ham.) T. Nees & Eberm using rat brain synaptosomes as model system.

The study investigated the perturbation of oxidant-antioxidant balance in brain synaptosomes of diabetic rats and determined the antioxidant and free radical-scavenging property of the Indian bay leaf. Brain synaptosomes were isolated from control and streptozotocin-induced diabetic animals and oxidative stress parameters were assayed. A methanolic extract of bay leaf (BLE) was tested for the polyphenolic content and antioxidant activity by in vitro assays. A significant increase in the levels of lipids and lipid peroxidation products and a decline in antioxidant potential were observed in diabetic rat brain synaptosomes. The total polyphenolic content of BLE was found to be 6.7 mg gallic acid equivalents (GAE)/100g. BLE displayed scavenging activity against superoxide and hydroxyl radicals in a concentration-dependent manner. Further, BLE showed inhibition of Fe(2+)-ascorbate induced lipid peroxidation in both control and diabetic rat brain synaptosomes. Maximum inhibition of lipid peroxidation, radical scavenging action and reducing power of BLE were observed at a concentration of 220 microg GAE. These effects of BLE in vitro were comparable with that of butylated hydroxyl toluene (BHT), a synthetic antioxidant. It can be concluded that synaptosomes from diabetic rats are susceptible to oxidative damage and the positive effects of bay leaf in vitro, could be attributed to the presence of antioxidant phytochemicals.

Lack of interaction of angiotensin converting enzyme inhibitors with muscarinic and neuropeptide Y receptors

In studies conducted in patients undergoing cardiac catheterizations, some hemodynamic changes were observed after the acute sublingual administration of the angiotensin converting enzyme inhibitors (ACEI) captopril, enalapril, and lisinopril. These changes consisted of an increase in pulmonary artery pressure, pulmonary vascular resistance (PVR) and induction of hypoxia. The pressure changes were transitory and disappeared after 25 min. The possible mechanisms involved in these changes may relate to interactions of the ACEI with peripheral receptor systems for hormones and neurotransmitters. We have thus undertaken the task of evaluating the potential effect of ACEI on biological receptor molecules. We have begun with studies on muscarinic receptors, and the recently characterized neuropeptide Y (NPY) receptors of endothelial cells. Equilibrium binding assays with 3H-QNB have been conducted for muscarinic receptors using rat brain synaptosomes, due to its expression of multiple muscarinic receptors subtypes. In addition 125BH-NPY binding assays were conducted on intact adrenal medullary endothelial cells. Enalapril and captopril, 10(-7) to 10(-3) M, were not able to produce significant inhibition of either muscarinic or NPY receptor probes. The paradoxical changes elicited by sublingual ACEI seems not to involve interaction with muscarinic or NPY receptors

Inhibition of acetylcholinesterase of mice erythrocytes & synaptosomes by dimethylsulfoxide.

In vitro inhibitory effect of dimethylsulfoxide (DMSO) on acetylcholinesterase of erythrocyte membranes and synaptosomes of mice was observed using acetylthiocholine as substrate. DMSO inhibited the enzyme from both sources and the effect was concentration dependent. It produced an inhibition of 26 to 28 per cent at a concentration of 0.13 mM and 92 to 95 per cent at a higher concentration of 1.91 mM. The Km of bound and solubilized enzyme of the synaptosomes was 0.2 and 0.15 mM while that of erythrocyte membranes 0.5 and 0.33 mM respectively. The Vmax was 0.4 and 0.4 (for synaptosomes) and 0.67 and 0.59 (for erythrocyte membranes) Mmoles/mg protein/min, respectively for bound and solubilized forms. The Ki of solubilized enzyme of synaptosomes was 0.11 mM. Kinetic studies showed that the inhibition was competitive in nature.

Effect of dexamethasone and reserpine on brain synaptosomal phosphorylation in lithium treated rats.

Increase in brain synaptosomal protein phosphorylation after lithium treatment was unaffected by prior treatment with dexamethasone, but decreased after reserpine administration indicating the involvement of neurotransmitters in lithium induced increase in synaptosomal phosphorylation.

Efeitos de neurotransmissores sobre a liberaçäo de LHRH imunorreativo de sinaptossomos hipotalâmicos do rato / Effects of neurotransmitters on immunoreactive LHRH liberation from rat hypothalamic synaptosomes

Estudos imuno-histoquímicos mostram a existência dos possíveis neurotransmissores serotonina (5-HT), ácido gama-aminobutírico (GABA) e histamina na eminência média hipotalâmica em concentraçöes elevadas. Pode-se assim supor sua participaçäo nos processos de secreçäo dos hormônios nessa regiäo, possivelmente através de interaçöes axo-axônicas. No presente trabalho foram estudados os efeitos da administraçäo desses neurotransmissores, a suspensöes incubadas de sinaptossomos do hipotálamo da rata, sobre a secreçäo do hormônio liberador das gonadotrofinas (LHRH). Verificamos que 5-HT, nas concentraçöes de 10**-4M e 10**-5M inibe a secreçäo desse hormônio e que o GABA também tem efeito inibitório, apenas em concentraçöes mais baixas (10**-6M e 10**-7M). A histamina näo teve efeito significante sobre a liberaçäo de LHRH. Como os resultados na literatura säo variáveis em termos de efeito excitatório ou inibitório dependendo das diversas condiçöes endócrinas do animal, sugere-se uma participaçäo dos hormônios esteróides gonadais na funçäo moduladora dos neurotransmissores, com respeito à sua açäo sobre a secreçäo do LHRH