Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.6.3.1 (Mg2+-ATPase)
 1,484 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Arsenic is a known global groundwater contaminant. The organochlorine insecticide endosulfan has gained significance as an environmental pollutant due to its widespread use in the control of many food- and non-food-crop-damaging insects. The adverse effects produced by arsenic or endosulfan alone in humans and animals are well documented, but very little is known about the consequences of their coexposure. We evaluated whether their simultaneous exposure can induce oxidative stress and affect antioxidative systems and certain membrane-bound enzymes in erythrocytes of broiler chickens. Day-old chicks were exposed to 3.7 ppm of arsenic via drinking water or 30 ppm of endosulfan-mixed feed or similarly coexposed to these in the same dose levels for 60 days. At term, the impact of their coexposure was assessed by evaluating lipid peroxidation (LPO), activities of superoxide dismutase (SOD), catalase, glutathione peroxidase (GPx), glutathione-S-transferase (GST), different ATPases and acetylcholinesterase (AChE) in erythrocytes, serum glucose, and levels of glutathione (GSH) and glycosylated hemoglobin (GHb) in blood. LPO was increased with all of the treatments. Catalase was decreased with endosulfan and the coexposure, but not with arsenic, whereas GSH was decreased with arsenic and endosulfan, but not with the coexposure. All of the treatments increased SOD and GPx activities. GST activity was increased only in the coexposed birds. None of the treatments affected the activities of total ATPase and Mg2+-ATPase. Na+-K+-ATPase activity was decreased in the endosulfan-treated and the coexposed birds. All three exposures increased erythrocyte AChE activity. Endosulfan increased the serum glucose level and arsenic and endosulfan increased GHb levels, but these were not altered in the coexposed birds. Erythrocyte protein content was insignificantly decreased with these treatments. Overall, the effects of coexposure were not appreciably different from either of the agents, except on AChE, GSH, and glucose. The results do not reflect any specific type of interaction between these agents in chicken erythrocytes, but they do indicate that the coexposure induces a low level of oxidative stress, which is comparable to that induced by arsenic or endosulfan.
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PMID:Effects of subchronic coexposure to arsenic and endosulfan on the erythrocytes of broiler chickens: a biochemical study. 1844 43

Manganese (Mn) is an essential metalloenzyme component that in high doses can exert serious oxidative and neurotoxic effects. The aim of this study was to investigate the potential effect of the antioxidant L-cysteine (Cys, 7 mg/kg) on the adult rat brain total antioxidant status (TAS) and the activities of acetylcholinesterase (AChE), Na+,K+-ATPase and Mg2+-ATPase induced by short-term Mn administration (as Mn chloride, 50 mg/kg). Twenty-eight male Wistar rats were divided into four groups: A (saline-treated control), B (Mn), C (Cys) and D (Mn and Cys). All rats were treated once daily, for 1 week with intraperitoneal injections of the tested compounds. Rats were killed by decapitation and mentioned parameters were measured spectrophotometrically. Rats treated with Mn exhibited a significant reduction in brain TAS (-39%, P < 0.001, B versus A) that was partially reversed by Cys co-administration (-13%, P < 0.01, D versus A), while Cys (group C) had no effect on TAS. The rat brain AChE activity was found significantly increased by both Mn (+21%, P < 0.001, B versus A) and Cys (+61%, P < 0.001, C versus A), while it was adjusted into the control levels by the co-administration of Mn and Cys. The activity of rat brain Na+,K+-ATPase was not affected by Mn administration, while Mg2+-ATPase exhibited a slight but statistically significant reduction in its activity (-9%, P < 0.01, B versus A) due to Mn, which was further reduced by Cys co-administration. The above findings suggest that short-term Mn in vivo administration causes a statistically significant decrease in the rat brain TAS and an increase in AChE activity. Both effects can be, partially or totally, reversed into the control levels by Cys co-administration (which could thus be considered for future applications as a neuroprotective agent against chronic exposure to Mn and the treatment of manganism). The activity of Na+,K+-ATPase is not affected by Mn, while Mg2+-ATPase activity is slightly (but significantly) inhibited by Mn, possibly due to Mg replacement.
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PMID:Effects of short-term exposure to manganese on the adult rat brain antioxidant status and the activities of acetylcholinesterase, (Na,K)-ATPase and Mg-ATPase: modulation by L-cysteine. 1881 1

Choline (Ch) plays an important role in brain neurotransmission, while Ch-deprivation (CD) has been linked to various pathophysiological states. Prolonged ingestion of Ch-deficient diet (CDD) is known to produce CD causing a reduction of rat brain acetylcholine (ACh) levels, as well as memory and growth disorders. The aim of this study was to investigate the effect of a 2-month adult-onset CD on the activities of acetylcholinesterase (AChE), (Na+,K+)- and Mg2+-ATPase in crucial brain regions of male rats. Adult rats were divided into two groups (control and CD). The CD group was fed with CDD for 2-months. At the end of the second month, rats were sacrificed by decapitation and the brain regions were rapidly removed. Enzyme activities were measured spectrophotometrically in the homogenated frontal cortex, hippocampus, hypothalamus, cerebellum, and pons. In CD rats, AChE activity was found statistically significantly increased in the hippocampus and the cerebellum (+28%, P<0.001 and +46%, P<0.001, respectively, as compared to control), while it was found unaltered in the other three regions (frontal cortex, hypothalamus and pons). (Na+,K+)-ATPase activity was found increased by CD in the frontal cortex (+30%, P<0.001), decreased in both hippocampus and hypothalamus (-68%, P<0.001 and -51%, P<0.001, respectively), and unaltered in both cerebellum and pons. No statistically significant changes were observed in the activities of Mg2+-ATPase in the frontal cortex and the hypothalamus, while statistically significant increases were recorded in the hippocampus (+21%, P<0.01), the cerebellum (+85%, P<0.001) and the pons (+19%, P<0.05), as compared to control levels. Our data suggest that adult-onset CD can have significant effects on the examined brain parameters in the examined crucial brain regions, as well as that CD is a metabolic disorder towards which different and brain region specific neurophysiological responses seem to occur. Following a 2-month adult-onset CD, the activity of AChE was found to be increased in the hippocampus and the cerebellum and unaltered in the other three regions (frontal cortex, hypothalamus and pons), while Na+,K+-ATPase activity was found to be increased in the frontal cortex, decreased in both hippocampus and hypothalamus, and unaltered in both cerebellum and pons. Moreover, Mg2+-ATPase activity was found to be unaltered in the frontal cortex and the hypothalamus, and increased in the hippocampus, the cerebellum and the pons. The observed differentially affected activities of AChE, (Na+,K+)-ATPase and Mg2+-ATPase (induced by CD) could result in modulations of cholinergic neurotransmission, neural excitability, metabolic energy production, Mg2+ homeostasis and protein synthesis (that might have a variety of neurophysiological consequences depending on the brain region in which they seem to occur).
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PMID:Effects of adult-onset choline deprivation on the activities of acetylcholinesterase, (Na+,K+)- and Mg2+-ATPase in crucial rat brain regions. 1899 98

Bombyx mori (B. mori), silkworm, is one of the most important economic insects in the world, while phoxim, an organophosphorus (OP) pesticide, impact its economic benefits seriously. Phoxim exposure can damage the brain, fatbody, midgut and haemolymph of B. mori. However the metabolism of proteins and carbohydrates in phoxim-exposed B. mori can be improved by Titanium dioxide nanoparticles (TiO2 NPs). In this study, we explored whether TiO2 NPs treatment can reduce the phoxim-induced brain damage of the 5th larval instar of B. mori. We observed that TiO2 NPs pretreatments significantly reduced the mortality of phoxim-exposed larva and relieved severe brain damage and oxidative stress under phoxim exposure in the brain. The treatments also relieved the phoxim-induced increases in the contents of acetylcholine (Ach), glutamate (Glu) and nitric oxide (NO) and the phoxim-induced decreases in the contents of norepinephrine (NE), Dopamine (DA), and 5-hydroxytryptamine (5-HT), and reduced the inhibition of acetylcholinesterase (AChE), Na+/K+-ATPase, Ca2+-ATPase, and Ca2+/Mg2+-ATPase activities and the activation of total nitric oxide synthase (TNOS) in the brain. Furthermore, digital gene expression profile (DGE) analysis and real time quantitative PCR (qRT-PCR) assay revealed that TiO2 NPs pretreatment inhibited the up-regulated expression of ace1, cytochrome c, caspase-9, caspase-3, Bm109 and down-regulated expression of BmIap caused by phoxim; these genes are involved in nerve conduction, oxidative stress and apoptosis. TiO2 NPs pretreatment also inhibited the down-regulated expression of H+ transporting ATP synthase and vacuolar ATP synthase under phoxim exposure, which are involved in ion transport and energy metabolism. These results indicate that TiO2 NPs pretreatment reduced the phoxim-induced nerve toxicity in the brain of B. mori.
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PMID:Molecular mechanisms of reduced nerve toxicity by titanium dioxide nanoparticles in the phoxim-exposed brain of Bombyx mori. 2497 66


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