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Introduction: Background Material
Published in Nassir H. Sabah, Neuromuscular Fundamentals, 2020
The CNS is chemically protected by the blood-brain barrier (BBB), which arises from tight junctions between the endothelial cells lining blood capillaries in the CNS. These tight junctions prevent the diffusion of bacteria and other large molecules from the blood into the extracellular space of the CNS. With few exceptions, only small fat-soluble molecules diffuse through the BBB. Substances that can diffuse through the BBB include alcohol, caffeine, nicotine, hormones, O2, and CO2, whereas other substances, including glucose, are actively transported through the BBB. The BBB prevents large drug molecules injected into the blood stream from reaching the cells of the CNS. On the other hand, the peripheral nervous system is vulnerable to neurotoxins because it is not chemically protected by a blood barrier.
Diseases of the Nervous System
Published in George Feuer, Felix A. de la Iglesia, Molecular Biochemistry of Human Disease, 2020
George Feuer, Felix A. de la Iglesia
Neurotoxic compounds cause a wide variety of effects on the nervous system. Many neurotoxins affect specific regions of the brain stem and produce toxic injury to specific cell functions or specific cell types. The site of action of several biological toxins on motor neurons has been established.473 The neuronal impairment can be selective producing an inhibition of protein synthesis, altering maintenance of the myelin structure, and blocking synaptic transmission, axonal transport, or conduction of action potentials.
The Evolutionary Significance of Drug Toxicity Over Reward
Published in Hanna Pickard, Serge H. Ahmed, The Routledge Handbook of Philosophy and Science of Addiction, 2019
Edward H. Hagen, Roger J. Sullivan
Central to our account of human drug use are the chemical defenses that evolved in marine and, later, in terrestrial autotrophs (plants). Some chemical defenses, such as tannins and other phenolics, have relatively non-specific effects on a wide range of molecular targets in the herbivore, for example binding to proteins and changing their conformation, thereby impairing their function. Other chemical defenses—neurotoxins—evolved to interfere specifically with signaling in the central nervous system (CNS) and peripheral nervous system. Various plant neurotoxins interfere with nearly every step in neuronal signaling, including (1) neurotransmitter synthesis, storage, release, binding, and re-uptake; (2) receptor activation and function; and (3) key enzymes involved in signal transduction. Plant neurotoxins have these effects, in many cases, because they have evolved to resemble endogenous neurotransmitters. Disruption of nervous system function by such toxins serves as a potent deterrent to herbivores (Wink 2011).
Virgin Coconut Oil-Induced Neuroprotection in Lipopolysaccharide-Challenged Rats is Mediated, in Part, Through Cholinergic, Anti-Oxidative and Anti-Inflammatory Pathways
Published in Journal of Dietary Supplements, 2021
Nur Syafiqah Rahim, Siong Meng Lim, Vasudevan Mani, Nurul Aqmar Mohamad Nor Hazalin, Abu Bakar Abdul Majeed, Kalavathy Ramasamy
Alzheimer’s disease (AD) is the leading cause of dementia amongst the elderly population (Um et al. 2012). It is characterised by progressive memory loss and deterioration in cognitive function (Lemere and Masliah 2010). The pathogenesis of AD hitherto remains poorly understood. Nevertheless, development and progression of AD were found to be associated with excessive aggregation of amyloid-β peptide (Aβ) derived from proteolysis of amyloid precursor protein (APP) (Dhanasekaran et al. 2009). Recent studies had further uncovered the correlation between oxidative stress and pathogenesis of AD (Zhang et al. 2010). Aβ could induce oxidative stress through mitochondrial dysfunction, which then result in increased reactive oxygen species (ROS). ROS is known to not only oxidise vital cellular components but also alter several signalling pathways including apoptosis through modulation of Bcl-2 and p53 proteins (Dypbukt et al. 1994; Brunet et al. 2001). As such, excessive production of ROS could cause cellular damage and subsequently cell death (Zhu et al. 2004). Besides, there is also increasing evidence that indicates the involvement of innate immune system in AD-related neuroinflammation. Activation of mononuclear phagocytic microglial cells could produce neurotoxic mediators such as reactive oxygen, nitrogen species and inflammatory cytokines. These neurotoxins would lead to neuronal cell death and give rise to chronic neurodegenerative conditions in AD (Walter et al. 2007).
Scorpion envenomation: a deadly illness requiring an effective therapy
Published in Toxin Reviews, 2021
Faez Amokrane Nait Mohamed, Fatima Laraba-Djebari
Several neurotoxins have been isolated after their chromatographic identification and biochemical characterization. α-type neurotoxins are highly active on Na+ channels in mammals and induce prolongation of the physical-chemical excitation, resulting in massive entry of Na+ into intracellular spaces and leading to an intense cellular depolarization (Figure 3) (Martin-Eauclaire et al.2005). Moreover, Buthidae venoms contain short toxins active on K+ channels, such as kaliotoxin (KTx) peptides of about 37 amino acids (Crest et al.1992, Laraba-Djebari et al.1994), as well as anti-insect toxins, such as Lqq IT 70 residues from Leiurus quinquestriatus quinquestriatus (Kopeyan et al.1990). β-type toxins acting on other sites of Na+ channels are isolated from African, American and Asian Buthidae venoms(Bechis et al.1984).
Identifying areas of improvement in nursing knowledge regarding hepatic encephalopathy management
Published in Journal of Community Hospital Internal Medicine Perspectives, 2021
Aalam Sohal, Victoria Green, Sunny Sandhu, Marina Roytman
- The pathophysiology of hepatic encephalopathy is multifactorial. The hypothesized neurotoxins include ammonia, tyramine, octopamine, manganese, GABA, etc., [1]; however, ammonia is the most widely recognised toxin. Ammonia is produced by the bacteria in the gastrointestinal tract and is cleared by liver. In the setting of cirrhosis, combination of declining liver function and portosystemic shunting leads to decreased ammonia clearance [11]. The ammonia crosses the blood brain leading to neuropsychiatric effects [12]. Although most of the nursing staff in our survey elected ammonia, some additionally chose urea which is not one of the toxins associated with OHE. We believe that improving the knowledge of the nursing staff on the pathogenesis of OHE would help in effective management of these complex patients during the hospitalization and after discharge.