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Outdoor Air Pollution
Published in William J. Rea, Kalpana D. Patel, Reversibility of Chronic Disease and Hypersensitivity, Volume 4, 2017
William J. Rea, Kalpana D. Patel
This depletion allows for the inability to handle the myriad of odors coming into the chemically sensitive individual. This then triggers a cascade of altered physiology response causing weakness, fatigue, and sensitivity to other foods and chemicals, nutrient need occurs. Considering the OS as a powerful promoter of other cellular pathways involved in disease processes and as a unique attendant in inflammatory responses, it has been put in the spotlight of the most mechanistic studies regarding the association of pesticide's exposure with chronic disorders. OS has been implicated in the onset and progression of pesticide-induced PD.157 In this regard, organochlorine pesticides have been reported to cause degeneration of dopaminergic neurons by an oxidative-dependent pathway in Parkinson's model.158,159 Additionally, disrupting effects of organophosphates on glucose homeostasis have been reportedly linked to oxidative damages and inflammatory CKs and thought to be compensatory responses accompanied with reduced insulin signaling in insulin-sensitive organs such as liver, muscle, and adipose tissue.160,161 As such, further disruption of glucose homeostasis in diabetic models of laboratory animals exposed to organophosphate insecticides has been associated with enhanced lipid peroxidation and decreased activity of AO enzymes.162 OS has also been reported to be involved in nephrotoxicity of some pesticides, including diazinon, acephate, and paraquat.163–165
Female infertility caused by organophosphates: an insight into the latest biochemical and histomorphological findings
Published in Toxin Reviews, 2023
Mohammad Samare-Najaf, Ali Samareh, Bahia Namavar Jahromi, Navid Jamali, Sina Vakili, Majid Mohsenizadeh, Cain C. T. Clark, Ali Abbasi, Nastaran Khajehyar
OPs-induced alterations in the expression of steroidogenic factor-1, a main regulator of steroid hormone biosynthesis, could disrupt the production of ovarian hormones (Armiliato et al.2014). Since the production of estradiol from testosterone requires the appropriate performance of aromatase, increasing ovarian testosterone levels and decreasing estradiol after exposure to OPs indicates the suppressive impact on the enzyme activity (Brandt et al.2015). Concerning the pivotal impact of ovarian hormones on the maturation of the oocytes, which is an irreplaceable step in the production of fertilizable eggs, acephate could interfere with the nongenomic action of progesterone on the meiotic maturation of oocytes, which is the activation of membrane-receptor associated second messengers, like cAMP or G proteins, through elevating the rate of germinal vesicle breakdown demonstrating the antiestrogenic role of OPs (Das and Thomas 1999, Tokumoto et al.2005, Ghodageri and Katti 2013). In addition to observing similar changes in the gestational embryonic ovary, a ban on sex steroids may be considered one of the main reasons (Ramana et al.1992). Unfortunately, long-term exposure to OPs causes mortality in addition to damaging ovarian tissue (Sumon et al.2019).
A new method for determining the benchmark dose tolerable region and endpoint probabilities for toxicology experiments
Published in Journal of Applied Statistics, 2020
Naha J. Farhat, Edward L. Boone, David J. Edwards
The proposed methods will be illustrated using the organophosphorus pesticides (OP) dataset from Moser et al. [17], who used lab experiments on rats to measure neurotoxicity as a result of exposure to pesticides commonly used in agriculture such as acephate, diazinon, dimethoate and malathion and using simulated data (see the supplementary material). Neurotoxicity for rats might be measured in terms of multiple endpoints or responses such as blood cholinesterase, brain cholinesterase, motor activity, and tail pinch, such that a decrease in any of these measurements is considered adverse. For simplicity in presentation, and to be able to visualize the tolerable region, our method is described only for the case of two stressors or chemicals exposure. We will discuss exposure to more than two stressors and visualizing multidimensional region in a separate manuscript.
Metabonomics analysis of serum from rats given long-term and low-level cadmium by ultra-performance liquid chromatography–mass spectrometry
Published in Xenobiotica, 2018
Liyan Hu, Lu Bo, Meiyan Zhang, Siqi Li, Xiujuan Zhao, Changhao Sun
Metabonomics is defined as “the quantitative measurement of the dynamic multiparametric metabolic response of living systems to pathophysiological stimuli or genetic modifications” (Nicholson et al., 1999), which can be used to measure the metabolic products of cells, tissues, organs or biological fluids (Beger & Sun, 2010; Roux et al., 2011). The application of metabolic profiling analysis can directly reveal the changes of small molecule metabolites and accurately reflect the status of biological systems (Nie et al., 2014). At the same time, metabonomics has shown great potential insight into disease processes, biomarker identification and toxicological mechanism (Lian et al., 2016; Xu et al., 2015). Currently, metabonomics has been widely used in the field of drug discovery and food safety (Mastrangelo et al., 2014; Rubert et al., 2015), which has become a useful tool in investigating the biochemical effects of toxic substances. For example, Hou et al. (2015) have studied the toxic effects of acephate administration on rats using ultra-performance liquid chromatography–mass spectrometry (UPLC–MS). The results indicated that exposure to acephate disrupted the metabolism of lipids and amino acids, induced oxidative stress, caused neurotoxicity and resulted in liver dysfunction.