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Adverse Effects and Intoxication with Essential Oils
Published in K. Hüsnü Can Başer, Gerhard Buchbauer, Handbook of Essential Oils, 2020
Neurotoxic effects include symptoms such as excitement, hallucinations, delirium, tremors, and convulsions (Opdyke, 1978). Camphor and camphor-containing essential oils have been included in the list of potential epileptogenics (Burkhard et al., 1999; Spinella, 2001).
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.
Gut Neuropeptides and the Pathophysiology of Inflammatory Bowel Disease
Published in William J. Snape, Stephen M. Collins, Effects of Immune Cells and Inflammation on Smooth Muscle and Enteric Nerves, 2020
Timothy R. Koch, Amnon Sonnenberg, J. Aidan Carney
This hypothesis has been derived from a large body of information produced by previous studies of IBD. The existence of genetic factors in development of IBD has been carefully examined, and the risk is much more pronounced in Crohn’s disease than in UC.32,33 As a component of our hypothesis, it is possible that genetic susceptibility could be related to the absence or presence of cell membrane constituents that allow binding of toxins to nervous tissue. In a recent epidemiologic study, we have shown that mortality data for IBD from the United States and the United Kingdom demonstrate a birth-cohort phenomenon, suggesting a changing exposure of consecutive generations to environmental influences.34 These environmental factors could be neurotoxic or could initiate pathways that eventually lead to neuronal damage.
Acrylamide induces intrinsic apoptosis and inhibits protective autophagy via the ROS mediated mitochondrial dysfunction pathway in U87-MG cells
Published in Drug and Chemical Toxicology, 2022
Linlin Deng, Mengyao Zhao, Yanan Cui, Quanming Xia, Lihua Jiang, Hao Yin, Liming Zhao
Acrylamide (ACR) is a chemical traditionally used as an industrial raw material in soil conditioning, wastewater treatment, and the textile industry (Erkekoglu and Baydar 2014). In addition, ACR has been revealed as a common food contaminant over the past 20 years (Mottram et al. 2002, Mesías et al. 2019). Exposure to ACR via dietary consumption, cigarette smoke, occupational settings, and other environmental sources can significantly affect human health (Bušová et al. 2020). Studies have shown that ACR displays various toxic effects, such as neurotoxicity, genotoxicity, reproductive toxicity, and potential carcinogenicity (Pundir et al. 2019). The neurotoxic properties have attracted the most research attention due to their pronounced toxic impact on humans (Zamani et al. 2017, Zhao et al. 2017b, Tan et al. 2019). A recent epidemiological study based on a prospective cohort conducted among 2534 nonsmoking elderly Chinese men showed that ACR exposure was associated with a mild cognitive decline and an increased risk of poor cognition over four years (Liu et al. 2017b). Early studies have confirmed that ACR at a dose of 0.5–50 mg/kg/day has been associated with various neurotoxic syndromes, such as weight loss, skeletal muscle weakness, and abnormal gait (Erkekoglu and Baydar 2014). Therefore, it has been used to mimic significant pathogenesis in patients with Alzheimer's disease and Parkinson's disease by inducing numerous biochemical and neuropathic events in the brain and spinal cord (LoPachin and Gavin 2012, Erkekoglu and Baydar 2014).
Emerging directions of cognitive aging with HIV: practice and policy implications for social work
Published in Journal of Gerontological Social Work, 2022
David E. Vance, Yookyong Lee, David Scott Batey, Wei Li, Crystal Chapman Lambert, Sai Rashmi Nakkina, Joseph N. Anderson, Kristen Triebel, Jun Y. Byun, Pariya L. Fazeli
Substance use damages cognitive reserve in several ways; however, it is important to note that the damaging effects can vary by dose, frequency of use, timed release or not, and individual differences. First, many substances create a neurotoxic environment and change gene expression in the brain, altering brain morphology (Korpi et al., 2015). Second, substance abuse is a risk factor for comorbidities such as hepatic, renal, and cardiovascular diseases (Sanchez & Kaul, 2017) and neuro-comorbidities can further tax brain physiology. Moreover, the synergistic effects of aging, HIV pathology, and substance use may be very damaging to the frontal lobes which tend to be more vulnerable to such insults; brain regions responsible for working memory and executive functioning (Sanchez & Kaul, 2017).
Developmental neurotoxicity of silver nanoparticles: the current state of knowledge and future directions
Published in Nanotoxicology, 2022
Lidia Strużyńska, Beata Dąbrowska-Bouta, Grzegorz Sulkowski
As the engineering of AgNPs and the utilization of AgNP-containing products by pregnant women, infants, and children rapidly increases, further targeted research is needed using models of exposure closely simulating environmental levels of AgNPs which are focused on dose-response effects and the underlying molecular mechanisms. One of the most important goals of future research is to determine the extent to which AgNPs can cause specific molecular alterations and to identify the behavioral correlates of such alterations. To predict possible effects of AgNPs exposure in the early periods of life, knowledge on molecular mechanisms is frequently extrapolated from studies using adult animals. This a priori assumption that the neurotoxic effects are similar regardless of the ‘time window’ of exposure, may prove incorrect, particularly in light of age-dependent physiological, morphological, and behavioral differences. Previous studies indicate that the neurodevelopmental consequences of toxic insult to the CNS are critically related to the time of exposure. Those occurring in the first half of gestation affect cytogenesis and histogenesis of the nervous system while those occurring during the second half of gestation and in the early postnatal period affect growth and differentiation of the brain (Trask and Kosofsky 2000).