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Hazard Characterization and Dose–Response Assessment
Published in Ted W. Simon, Environmental Risk Assessment, 2019
The difference between toxicodynamics and toxicokinetics is evident in a very recent risk assessment of the organophosphate (OP) pesticide chlorpyrifos. The MOA for OPs is well known—inhibition of cholinesterases, with toxicity manifested as central and peripheral cholinergic effects.200 Thionophosphorus OPs such as chlorpyrifos do not directly inhibit acetyl cholinesterase (AChE), but must first be metabolized to the oxygen analog, or oxon, by CYP450 mixed-function oxidases, mainly occurring in the liver. Paraoxonase 1 (PON1) is an arylesterase that metabolizes organophosphate compounds. Chlorpyrifos oxon is inactivated by the enzyme paraoxonase (PON1) in the liver and other tissues,201,202 Genetic polymorphisms exist in the PON1 gene, and lifestyle factors such as the use of cholesterol-lowering medications and alcohol consumption may increase PON1 activity.203–206
Protein-Based Bioscavengers of Organophosphorus Nerve Agents
Published in Brian J. Lukey, James A. Romano, Salem Harry, Chemical Warfare Agents, 2019
Moshe Goldsmith, Yacov Ashani, Tamara. C. Otto, C. Linn Cadieux, David. S. Riddle
The notion of a protein bioscavenger is not a novel concept. In the late 1950s, A.R. Main demonstrated that an exogenous injection of an arylesterase provides protection against multiple LD50s of parathion in rats (Main, 1956). Because the bioscavenger can inactivate nerve agents before these toxic compounds inhibit AChE, early scavenger administration could avoid the onset of a toxic insult from nerve agent poisoning. While research has demonstrated the utility of this approach in vivo, stoichiometric bioscavengers have one main disadvantage in that once phosphylated by a molecule of nerve agent, the enzyme is unable to bind to another nerve agent molecule. As a result, the level of protection is directly proportional to the concentration of unbound, active bioscavenger in circulation. Therefore, a high concentration of stoichiometric bioscavenger is required to protect against multiple LD50s of a nerve agent exposure (Ashani and Pistinner, 2004; Lenz et al., 2007).
High Carbohydrate Diet-Induced Metabolic Syndrome in the Overweight Body
Published in Nilanjana Maulik, Personalized Nutrition as Medical Therapy for High-Risk Diseases, 2020
Turan’s group and others emphasized that MetS is also characterized with increased oxidative stress, a condition due to an imbalance between production and scavenging of oxidants in the antioxidant system (Vendemiale, Guerrieri et al. 1995; Bonomini, Rodella et al. 2015; Okatan, Tuncay et al. 2015; Bhatti, Bhadada et al. 2016; Gregorio, De Souza et al. 2016). Increased oxidative stress can play an important role in the pathogenesis of various diseases including MetS (Roberts and Sindhu 2009; Bonomini, Rodella et al. 2015), in part due to its amplification by a concomitant antioxidant deficiency which may favor the propagation of oxidative alterations from intra- to extracellular spaces. Similar to other studies (Galassetti 2012; Korkmaz, Altinoglu et al. 2013; Okatan, Tuncay et al. 2015), our findings, related with significantly increased total oxidative status and decreased total antioxidant status in sera of rats with MetS, support these statements. These changes may further affect the impairment of insulin signaling, which further leads to insulin resistance. Indeed, previous studies using a high sucrose diet have shown a marked glucose intolerance in MetS modeled experimental animals (Pagliassotti, Prach et al. 1996; Brenner, Rimoldi et al. 2003). Additionally, they have shown significantly decreased serum paraoxonase and arylesterase activities in MetS group. Since the antioxidant properties of HDLs are attributable to serum paraoxonase and arylesterase activities (James 2006), these activities seem to be crucial in the relation to increased oxidative stress and organ dysfunction, particularly in terms of cardiovascular pathologies in rats with MetS (Kagota, Maruyama et al. 2013; Eren, Abuhandan et al. 2014).
Effect of certain non-steroidal anti-inflammatory drugs on the paraoxonase 2 (PON2) in human monocytic cell line U937
Published in Archives of Physiology and Biochemistry, 2018
Ayla Solmaz Avcıkurt, Oğuzhan Korkut
The in vitro effects of commonly used NSAIDs, Tenoxicam and Diclofenac sodium, on the enzymatic activity of PON2 were studied (Figure 1). These drugs were applied to human monocytic cell line U937, and their PON2-specific lactonase activities were then determined. Use of diclofenac sodium led to a significant decline in the lactonase activity during the incubation of 6–12 h in 1.69 mM dose (Figure 2(B)). Tenoxicam reduced the lactonase activity during the incubation time of 6 h in 0.74 mM dose (Figure 3(B)). The activity of arylesterase was examined in this study, as well. Diclofenac sodium didn’t make any change in the arylesterase activity (Figure 2(A)). On the other hand, tenoxicam decreased arylesterase activity during the use of 12 h, in 0.74 mM and 1.48 mM dose (Figure 3(A)). Although the arylesterase and lactonase activities decreased at the other doses, it was not statistically significant.
Serum paraoxonase activity in patients with ischaemic and nonischaemic dilated cardiomyopathy
Published in Acta Cardiologica, 2018
Fatih Gungoren, Tunay Senturk, Alper Ozturk, Kerem Koz, Emre Sarandol, Dilek Yesilbursa, Sumeyye Gullulu, Guven Ozkaya, Ali Aydinlar
Clinical studies, as well as experimental studies, have demonstrated that oxidative stress plays a pivotal role in the pathogenesis of heart failure. Tang et al. [9] evaluated serum arylesterase activity in patients with impaired left ventricular systolic function and found that 68% of patients with heart failure had an ischaemic aetiology. They divided patients into two groups according to serum arylesterase activity (<121 mol/L/min/mL and ≥121 mol/L/min/mL). Tang et al. [9] found that patients with systolic heart failure had reduced serum arylesterase activity, a marker of oxidative stress, and they also demonstrated that patients with systolic heart failure had reduced serum arylesterase activity that was a strong predictor of poorer outcomes. These results were consistent with both ischaemic and nonischaemic heart failure. A study by Kim et al. [10] showed that the activity of PON1 was significantly reduced in patients with HF, 39% of whom had an ischaemic aetiology, compared with the control subjects. Karabacak et al. [11] measured total antioxidant capacity and total oxidative status in patients with nonischaemic heart failure and also showed that oxidative stress levels were higher in HF patients. Hill et al. [18] showed that HF subsequent to myocardial infarction was associated with reduced superoxide dismutase levels, glutathione peroxidase levels, catalase activities, and vitamin E levels and with increased oxidative stress in rats. However, to date, no study has compared serum PON1 activities in patients with IDCM and NDCM. Our study investigated whether serum PON1 activity was different between patients with IDCM or NDCM.
Chemoprotection by Kolaviron of Garcinia kola in Benzene-induced leukemogenesis in Wistar rats
Published in Egyptian Journal of Basic and Applied Sciences, 2022
Olaniyi Solomon Ola, Esther Oladayo Ogunkanmbi, Emmanuel Babatife Opeodu
Plasma AOPP was determined by the method described by Witko et al. [26] as modified by Zhang et al. [27]. Briefly, plasma (100 μl) was added to 400 μl of phosphate buffer saline (PBS) solution and 25 μl of 1.16 M potassium iodide was then added followed 2 min later by 50 μl of acetic acid. The absorbance of the reaction mixture was immediately read at 340 nm against a blank containing 500 μl of PBS, 25 μl of 1.16 M potassium iodide and 50 μl of acetic acid. Plasma total thiol was measured spectrophotometrically using DTNB (2,2’-dinitro-5,5’-dithiodibenzoic acid) [28]. Arylesterase activity was determined using phenylacetate as the substrate following the procedure described by Erdem et al. [29].