scholarly journals Exposure to the organophosphorus pesticide chlorpyrifos inhibits acetylcholinesterase activity and affects muscular integrity in Xenopus laevis larvae

Chemosphere ◽  
2005 ◽  
Vol 61 (11) ◽  
pp. 1665-1671 ◽  
Author(s):  
Anita Colombo ◽  
Federica Orsi ◽  
Patrizia Bonfanti
The Analyst ◽  
2016 ◽  
Vol 141 (5) ◽  
pp. 1830-1836 ◽  
Author(s):  
Xiuzhong Wang ◽  
Shanshan Dong ◽  
Ting Hou ◽  
Lei Liu ◽  
Xiaojuan Liu ◽  
...  

A homogeneous electrochemical strategy for the detection of organophosphorus pesticides based on the inhibition of acetylcholinesterase activity and configuration change of hairpin DNA probes was developed.


1989 ◽  
Vol 67 (10) ◽  
pp. 1183-1189 ◽  
Author(s):  
C. G. Rousseaux ◽  
A. K. Dua

HI-6 is an oxime experimentally developed for reactivation of previously untreatable soman-phosphorylated acetylcholinesterase. It has been shown to be effective in restoring acetylcholinesterase activity after poisoning with other "nerve agents" namely VX and sarin; however, its antidotal qualities for the treatment of organophosphorus pesticide poisoning are not well known. HI-6, and other H-series oximes, apparently act in a number of ways: reactivation of acetylcholinesterase, blockage of ganglia and muscarinic receptors, stimulation of vasopressor and respiratory centre receptors, chemical combination with agents, restoration of neuromuscular transmission, retardation of the formation of the aged inhibitor–enzyme complex, and (or) inhibition of the release of acetylcholine.Key words: HI-6, H-series oxime, acetylcholinesterase, soman, mechanisms.


Neuroscience ◽  
1983 ◽  
Vol 10 (4) ◽  
pp. 1487-1495 ◽  
Author(s):  
C.B. Gundersen ◽  
R. Miledi

2013 ◽  
Vol 33 (3) ◽  
pp. 251-263 ◽  
Author(s):  
S Karami-Mohajeri ◽  
MR Hadian ◽  
S Fouladdel ◽  
E Azizi ◽  
MH Ghahramani ◽  
...  

Muscle dysfunction in acute organophosphorus (OP) poisoning is a cause of death in human. The present study was conducted to identify the mechanism of action of OP in terms of muscle mitochondrial dysfunction. Electromyography (EMG) was conducted on rats exposed to the acute oral dose of malathion (400 mg/kg) that could inhibit acetylcholinesterase activity up to 70%. The function of mitochondrial respiratory chain and the rate of production of reactive oxygen species (ROS) from intact mitochondria were measured. The bioenergetic pathways were studied by measurement of adenosine triphosphate (ATP), lactate, and glycogen. To identify mitochondrial-dependent apoptotic pathways, the messenger RNA (mRNA) expression of bax and bcl-2, protein expression of caspase-9, mitochondrial cytochrome c release, and DNA damage were measured. The EMG confirmed muscle weakness. The reduction in activity of mitochondrial complexes and muscular glycogen with an elevation of lactate was in association with impairment of cellular respiration. The reduction in mitochondrial proapoptotic stimuli is indicative of autophagic process inducing cytoprotective effects in the early stage of stress. Downregulation of apoptotic signaling may be due to reduction in ATP and ROS, and genotoxic potential of malathion. The maintenance of mitochondrial integrity by means of artificial electron donors and increasing exogenous ATP might prevent toxicity of OPs.


Author(s):  
Darcy B. Kelley ◽  
Martha L. Tobias ◽  
Mark Ellisman

Brain and muscle are sexually differentiated tissues in which masculinization is controlled by the secretion of androgens from the testes. Sensitivity to androgen is conferred by the expression of an intracellular protein, the androgen receptor. A central problem of sexual differentiation is thus to understand the cellular and molecular basis of androgen action. We do not understand how hormone occupancy of a receptor translates into an alteration in the developmental program of the target cell. Our studies on sexual differentiation of brain and muscle in Xenopus laevis are designed to explore the molecular basis of androgen induced sexual differentiation by examining how this hormone controls the masculinization of brain and muscle targets.Our approach to this problem has focused on a highly androgen sensitive, sexually dimorphic neuromuscular system: laryngeal muscles and motor neurons of the clawed frog, Xenopus laevis. We have been studying sex differences at a synapse, the laryngeal neuromuscular junction, which mediates sexually dimorphic vocal behavior in Xenopus laevis frogs.


2016 ◽  
Vol 86 (1-2) ◽  
pp. 36-47 ◽  
Author(s):  
Imen Dridi ◽  
Nidhal Soualeh ◽  
Torsten Bohn ◽  
Rachid Soulimani ◽  
Jaouad Bouayed

Abstract.This study examined whether perinatal exposure to polluted eels (Anguilla anguilla L.) induces changes in the locomotor activity of offspring mice across lifespan (post-natal days (PNDs) 47 – 329), using the open field and the home cage activity tests. Dams were exposed during gestation and lactation, through diets enriched in eels naturally contaminated with pollutants including PCBs. Analysis of the eel muscle focused on the six non-dioxin-like (NDL) indicator PCBs (Σ6 NDL-PCBs: 28, 52, 101, 138, 153 and 180). Four groups of dams (n = 10 per group) received either a standard diet without eels or eels (0.8 mg/kg/day) containing 85, 216, or 400 ng/kg/day of ϵ6 NDL-PCBs. The open field test showed that early-life exposure to polluted eels increased locomotion in female offspring of exposed dams but not in males, compared to controls. This hyperlocomotion appeared later in life, at PNDs 195 and 329 (up to 32 % increase, p < 0.05). In addition, overactivity was observed in the home cage test at PND 305: exposed offspring females showed a faster overall locomotion speed (3.6 – 4.2 cm/s) than controls (2.9 cm/s, p <0.05); again, males remained unaffected. Covered distances in the home cage test were only elevated significantly in offspring females exposed to highest PCB concentrations (3411 ± 590 cm vs. 1377 ± 114 cm, p < 0.001). These results suggest that early-life exposure to polluted eels containing dietary contaminants including PCBs caused late, persistent and gender-dependent neurobehavioral hyperactive effects in offspring mice. Furthermore, female hyperactivity was associated with a significant inhibition of acetylcholinesterase activity in the hippocampus and the prefrontal cortex.


Planta Medica ◽  
2012 ◽  
Vol 78 (11) ◽  
Author(s):  
A Landreau ◽  
S Bertrand ◽  
C Simoes-Pires ◽  
L Marcourt ◽  
TD Bach ◽  
...  

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