Influence of trimedoxime and atropine on acetylcholinesterase activity in some parts of the brain of mice poisoned by isopropylmethyl phosphonofluoridate

It has been established that the non-neuronal cholinergic system is related to the oncogenesis which increases the attractiveness of its components as the promising markers of oncologic diseases. The purpose of this work is to evaluate the clinical significance of the analysis of the activity of acetyl cholinesterase as a new marker of gliomas. The activity of acetyl cholinesterase was assessed by photo colorimetric analysis according to the Hestrin method recalculating the activity of the enzyme in the tumor tissue per 1 g of protein, and in the blood - by 0.1 g of hemoglobin. The data obtained in the primary tumors of the brain (28) in the tissue of the brain of persons who died as a result of injury (6) and in whole blood of patients with gliomas (28) and practically healthy people (10) were compared with the use of a number of statistical programs. A significant decrease in the activity of acetyl cholinesterase in tumor tissue and in whole blood is revealed as the degree of anaplasia of tumors increases, starting with Grade II. It is for the first time that a significant direct correlation was noted showing the consistency between the decrease in the activity of acetyl cholinesterase in the tumor tissue of the brain and blood. Bioinformatic analysis showed the connection of the enzyme of acetyl cholinesterase with proteins of the PI3K-AKT and Notch signaling pathways providing antiapoptotic and proliferative effects. The found dependences provide new insights into understanding of the mechanisms of gliomas genesis and can be used for selection of new diagnostic markers of brain tumors.

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A Tracer Kinetic Model for Measurement of Regional Acetylcholinesterase Activity in the Brain Using [11C]Physostigmine and PET

Physiological Imaging of the Brain with PET ◽

10.1016/b978-012285751-5/50042-9 ◽

2001 ◽

pp. 273-278

Author(s):

G. Blomvist ◽

B. Tavitian ◽

S. Pappata ◽

C. Crouzel ◽

A. Jobert ◽

...

Keyword(s):

Kinetic Model ◽

Acetylcholinesterase Activity ◽

Tracer Kinetic ◽

The Brain

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Biomarker Effects in Carassius auratus Exposure to Ofloxacin, Sulfamethoxazole and Ibuprofen

International Journal of Environmental Research and Public Health ◽

10.3390/ijerph16091628 ◽

2019 ◽

Vol 16 (9) ◽

pp. 1628 ◽

Cited By ~ 4

Author(s):

Xiaofan Yang ◽

Xiaoping Xu ◽

Xueyu Wei ◽

Jie Wan ◽

Yu Zhang

Keyword(s):

Ache Activity ◽

Carassius Auratus ◽

Crucian Carp ◽

Hazard Quotient ◽

Acetylcholinesterase Activity ◽

Response To Treatment ◽

Aquatic Environments ◽

Combined Effects ◽

Adverse Impacts ◽

The Brain

Ofloxacin, sulfamethoxazole and ibuprofen are three commonly used drugs which can be detected in aquatic environments. To assess their ecotoxicity, the effects of these three pharmaceuticals and their mixture on AChE (acetylcholinesterase) activity in the brain, and EROD (7-ethoxyresorufin-O-deethylase) and SOD (superoxide dismutase) activities in the liver of the freshwater crucian carp Carassius auratus were tested after exposure for 1, 2, 4 and 7 days. The results showed that treatments with 0.002–0.01 mg/L ofloxacin and 0.0008–0.004 mg/L sulfamethoxazole did not significantly change AChE, EROD and SOD activities. AChE activity was significantly inhibited in response to treatment with >0.05mg/L ofloxacin and >0.02 mg/L sulfamethoxazole. All three biomarkers were induced significantly in treatments with ibuprofen and the mixture of the three pharmaceuticals at all the tested concentrations. The combined effects of ofloxacin, sulfamethoxazole and ibuprofen were compared with their isolated effects on the three biomarkers, and the results indicated that exposure to ibuprofen and the mixture at environmentally relevant concentrations could trigger adverse impacts on Carassius auratus. The hazard quotient (HQ) index also demonstrated a high risk for ibuprofen. Moreover, the present study showed that the effects of ofloxacin, sulfamethoxazole and ibuprofen might be additive on the physiological indices of Carassius auratus.

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Walnut Oil Prevents Scopolamine-Induced Memory Dysfunction in a Mouse Model

Molecules ◽

10.3390/molecules25071630 ◽

2020 ◽

Vol 25 (7) ◽

pp. 1630

Author(s):

Jianqiao Liao ◽

Yifan Nai ◽

Li Feng ◽

Yimeng Chen ◽

Mei Li ◽

...

Keyword(s):

Body Weight ◽

Memory Impairment ◽

Acetylcholinesterase Activity ◽

Walnut Oil ◽

Histological Changes ◽

Hippocampal Ca1 ◽

Malondialdehyde Content ◽

Wet Weight ◽

The Brain ◽

Total Superoxide Dismutase

For thousands of years, it has been widely believed that walnut is a kind of nut that has benefits for the human body. Walnut oil, accounting for about 70% of walnut, mainly consists of polyunsaturated fatty acids. To investigate the effect of walnut oil on memory impairment in mice, scopolamine (3 mg/kg body weight/d) was used to establish the animal model during Morris Water Maze (MWM) tests. Walnut oil was administrated orally at 10 mL/kg body weight/d for 8 consecutive weeks. The results showed that walnut oil treatment ameliorated the behavior of the memory-impaired mice in the MWM test. Additionally, walnut oil obviously inhibited acetylcholinesterase activity (1.26 ± 0.12 U/mg prot) (p = 0.013) and increased choline acetyltransferase activity (129.75 ± 6.76 U/mg tissue wet weight) in the brains of scopolamine-treated mice (p = 0.024), suggesting that walnut oil could prevent cholinergic function damage in mice brains. Furthermore, walnut oil remarkably prevented the decrease in total superoxide dismutase activity (93.30 ± 5.50 U/mg prot) (p = 0.006) and glutathione content (110.45 ± 17.70 mg/g prot) (p = 0.047) and the increase of malondialdehyde content (13.79 ± 0.96 nmol/mg prot) (p = 0.001) in the brain of scopolamine-treated mice, indicating that walnut oil could inhibit oxidative stress in the brain of mice. Furthermore, walnut oil prevented histological changes of neurons in hippocampal CA1 and CA3 regions induced by scopolamine. These findings indicate that walnut oil could prevent memory impairment in mice, which might be a potential way for the prevention of memory dysfunctions.

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