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Background: The cholinergic neurotransmission within the human mesenteric lymphatic vessels has been poorly studied. Therefore, our aim is to analyse the cholinergic nerve fibres of lymphatic vessels using the traditional enzymatic techniques of staining, plus the biochemical modifications of acetylcholinesterase (AChE) activity. Materials and methods: Specimens obtained from human mesenteric lymphatic vessels were subjected to the following experimental procedures: 1) drawing, cutting and staining of tissues; 2) staining of total nerve fibres; 3) enzymatic staining of cholinergic nerve fibres; 4) homogenisation of tissues; 5) biochemical amount of proteins; 6) biochemical amount of AChE activity; 6) quantitative analysis of images; 7) statistical analysis of data. Results: The mesenteric lymphatic vessels show many AChE positive nerve fibres around their wall with an almost plexiform distribution. The incubation time was performed at 1 h (partial activity) and 6 h (total activity). Moreover, biochemical dosage of the same enzymatic activity confirms the results obtained with morphological methods. Conclusions: The homogenates of the studied tissues contain strong AChE activity. In our study, the lymphatic vessels appeared to contain few cholinergic nerve fibres. Therefore, it is expected that perivascular nerve stimulation stimulates cholinergic nerves innervating the mesenteric arteries to release the neurotransmitter AChE, which activates muscarinic or nicotinic receptors to modulate adrenergic neurotransmission. These results strongly suggest, that perivascular cholinergic nerves have little or no effect on the adrenergic nerve function in mesenteric arteries. The cholinergic nerves innervating mesenteric arteries do not mediate direct vascular responses. (Folia Morphol 2013; 72, 4: 322–327)
Lately, different therapy strategies for treating or slowing the progression of Alzheimer's disease are being analyzed. Moreover, the last two decades have seen a considerable research effort directed towards discovering the causes of Alzheimer's disease with the ultimate hope of developing safe and effective pharmacological treatments. In addition to the therapeutic strategies based on targeted drugs, the regimens will require the simultaneous application of neuroprotective drugs. Therefore, although there is currently no "cure" for Alzheimer's disease, a large number of potential therapeutic strategies emerged lately. In this small mini-review we will selectively describe some of the compounds derived from plants that could have a great potential in the treatment of various diseases, including Alzheimer's disease. In this way, there are many plant species that have been traditionally used for memory disorders. The differentiated results and powerful activity of these extracts are making these neuroprotective strategies to be somehow plausible for the treatment of Alzheimer's disease. In addition, these plants can be examined in order to isolate and identify their active ingredients and this can serve as a starting point to find safer and more effective agents for therapeutic use. On thing is certain: as the effective treatment options are limited, there is a demand for new drugs. Thus, plant extracts or vegetal compounds could represent an important part in this equation.
Acetylcholinesterase (AChE) sequentially extracted from mature specimens of Hymenolepis diminuta was shown to be a globular protein, the monomeric form of which (Ga₁) had molecular mass of 66 kDa as determined by SDS-PAGE. Amphiphilic character of the enzyme was revealed by Triton X-l14 phase partitioning. The cestode AChE preferred acetylthiocholine over propionyl- and butyrylthiocholine as substrate, split N-acetyl-ß-methylthiocholine and myristoylcholine but did not hydrolyze ß-carbonaphthoxycholine, a substrate for butyrylcholinesterases. It was sensitive to 10⁻⁵ M physostigmine and 10⁻⁵ M BW284C51 but not to 10⁻³ M iso-OMPA. No butyrylcholinesterase activity was detected in extracts from the parasite.
An active biomonitoring study was carried out on the Algerian west coast using wild reference mussels (Mytilus galloprovincialis) sampled from the Kristel (K) site and transplanted in net cages during one month (between May and June 2007) to Oran Harbour (OH) and Mostaganem Harbour (MH), areas characterised by high levels of urban and industrial pollution. The biological response of the mussels was evaluated by their condition index and the use of a general stress biomarker (evaluation of lysosomal membrane stability: the neutral red retention time (NRRT) method), a genotoxic effects biomarker (determination of micronuclei (MN) frequency) and a neurotoxic effects biomarker (determination of the acetylcholinesterase (AChE) concentration). Compared to the K reference specimens, OH and MH caged mussels presented a significant decrease of NRRT in lysosomal haemocytes (56.45±26.48 min and 67.25±22.77 min, respectively) (78±16.97 min for K mussels), an MN frequency respectively 7.3 and 9 times higher in the haemocytes and the gill cells of the OH caged mussels, and 7.2 and 6.4 times higher in the two tissues of the MH caged mussels. Significant inhibition of AChE activity was noted in the gills (16.93±3.1 nmol min−1 mg prot−1) and the digestive gland (7.69±1.79 nmol min−1 mg prot−1) of the OH mussels, but only in the gills (23.21±5.94 nmol min−1 mg prot−1) of the MH mussels, compared to the organs of the K control specimens (35.9±6.4 nmol min−1 mg prot−1 in the gills and 11.17±0.49 nmol min−1 mg prot−1 in the digestive gland). This study reflects the interest in such in situ biomonitoring assays and the utility of these biomarkers for assessing the effects of pollution in the Algerian coastal marine environment.
The erythrocytes of 12-month old Sod1 −/− mice showed an increased level of reactive oxygen species (ROS), as estimated by the degree of dihydroethidine and dihydrorhodamine oxidation, and the increased level of Heinz bodies. No indices of severe oxidative stress were found in the red blood cells and blood plasma of Sod1 −/− mice as judged from the lack of significant changes in the levels of erythrocyte and plasma glutathione, plasma protein thiol and carbonyl groups and thiobarbituric-acid reactive substances in the blood plasma. However, a decreased erythrocyte lifespan, increased reticulocyte count and splenomegaly were noted, indicating the importance of superoxide dismutase for maintaining erythrocyte viability. The levels of erythrocyte ROS and Heinz bodies and the reticulocyte count were indistinguishable in Sod1 +/+ and Sod1 +/− mice, suggesting that a superoxide dismutase activity decrease to half of its normal value may be sufficient to secure the protective effects of the enzyme.
This study was intendent to examine if N-acetylcysteine (NAC) changes liver GSH levels and influences ChE serum activity in rats intoxicated with chlorfenvinphos. The studies were conducted on male Wistar rats of 200±20 g body weight. One group of rats was pretreated with 0.1% water solution of NAC. NAC was administered in drinking water 24h before intoxication. The control groups received oil intragastrically by stomach tube in the amount of 0.1ml/100g (I), immediately or after NAC pretreatment. The experimental groups received oil solution of chlorfenvinphos in a dose of 0.02 LD50 or 0.1 LD50 immediately or after pretreatment with NAC. One and 24 hours after intoxication with chlorfenvinphos (or after NAC pretreatment) the blood samples were collected and livers were quickly removed and placed in iced 0.9% NaCl containing 0.16 mg/ml heparin. ChE serum activity and GSH level were measured. The results of this study demonstrated the changes in serum ChE activity and liver glutathione levels in the rats after administration of chlorfenvinphos at single doses. The results reported here indicate that NAC influences a decreased level of GSH in the liver of chlorfenvinphos-intoxicated rats and does not prevent ChE inhibition.
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