Study of paraoxonase-1 function on tissue damage of dichlorvos

Wang, Nana; Dai, Huaping; Li, Yuan; Han, Zhenkun; Sun, Jian-bo; Zhang, Zhigang; Zhao, Min

doi:10.1016/j.toxlet.2010.04.008

Cited by 8 publications

(6 citation statements)

References 8 publications

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“…Studies also implicated exposure to organophosphates in the development and progression of the motor and cognitive symptoms in Parkinson's disease, especially in subjects with the PON1L55M genotype, the slow metabolizer variant of PON-1 [48]. On the other hand, the administration of exogenous PON-1 to rats and mice could protect against organophosphate toxicity [43,49]. As shown in the present work, the administration of brilliant blue G to malathion-intoxicated rats resulted in a significant increase in PON-1 enzyme activity.…”

Section: Rosmentioning

confidence: 99%

Novel Protective Effects of Brilliant Blue G in Acute Malathion Toxicity

Abdel-Salam

Sleem

Youness

et al. 2018

ROS

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We investigated the effect of brilliant blue G on the development of oxidative stress and tissue damage in rats with acute malathion intoxication. Rats received a single dose of malathion (150 mg/kg) intraperitoneally (ip) and then treated with either saline or brilliant blue G (5, 10, or 20 mg/kg, ip). The control group received saline. Rats were euthanized 4 h after the last injection, and the brain and liver were removed for biochemical studies including determination of the lipid peroxidation malondialdehyde (MDA), nitric oxide, reduced glutathione (GSH), paraoxonase-1 (PON-1), butyrylcholinesterase (BChE), and Na +-K + ATPase activities. Histopathological evaluation of the brain and liver tissue was also performed. Results indicated that rats treated with only malathion exhibited significantly increased MDA and nitric oxide in the brain and liver accompanied with significant decline in tissue levels of GSH. In addition, there was significant decline in brain and liver PON-1 activity and a significantly decreased brain BChE and Na +-K + ATPase activities. Brilliant blue G at doses of 5-20 mg/kg caused a dose-dependent decrease in MDA, and at doses of 10-20 mg/kg decreased nitric oxide, and increased GSH in the brain and liver of malathion-treated rats. It also increased PON-1 activity in the brain (at doses of 10-20 mg/kg) and liver (at a dose of 20 mg/kg). Brilliant blue G at doses of 5-20 mg/kg increased BChE activity and at doses of 10-20 mg/kg increased Na +-K +-ATPase activity in the brain of malathion-treated rats. In conclusion, treatment with brilliant blue G decreased oxidative stress in the brain and liver and restored BChE and Na +-K + ATPase activities in the brain of malathion-intoxicated rats. The dye afforded protection against malathion-induced neuronal and liver cell injury.

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Section: Rosmentioning

confidence: 99%

Novel Protective Effects of Brilliant Blue G in Acute Malathion Toxicity

Abdel-Salam

Sleem

Youness

et al. 2018

ROS

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“…of Pages 6 2 M. Valiyaveettil et al / Toxicology Letters xxx (2011) xxx-xxx et al, 2005bFurlong et al, 2005;Li et al, 1995;Otto et al, 2009;Otto et al, 2010;Rochu et al, 2007;Stevens et al, 2008). Most of these studies were either performed under in vitro conditions, or in rodent models of OP toxicity (Duysen et al, 2010;Fu et al, 2005;Li et al, 1995;Wang et al, 2010). We also reported efficient hydrolysis of the CWNA tabun in comparison to sarin and soman by PON1 using in vitro analysis (Valiyaveettil et al, 2010).…”

Section: G Modelmentioning

confidence: 78%

Recombinant paraoxonase 1 protects against sarin and soman toxicity following microinstillation inhalation exposure in guinea pigs

Valiyaveettil

Alamneh

Rezk³

et al. 2011

Toxicology Letters

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Valiyaveettil, Manojkumar; Alamneh, Yonas; Rezk, Peter; Perkins, Michael W.; Sciuto, Alfred M.; Doctor, Bhupendra P.; and Nambiar, Madhusoodana P., "Recombinant paraoxonase 1 protects against sarin and soman toxicity following microinstillation inhalation exposure in guinea pigs" (2011 b s t r a c tTo explore the efficacy of paraoxonase 1 (PON1) as a catalytic bioscavenger, we evaluated human recombinant PON1 (rePON1) expressed in Trichoplusia ni larvae against sarin and soman toxicity using microinstillation inhalation exposure in guinea pigs. Animals were pretreated intravenously with catalytically active rePON1, followed by exposure to 1.2 X LCt 50 sarin or soman. Administration of 5 units of rePON1 showed mild increase in the blood activity of the enzyme after 30 min, but protected the animals with a significant increase in survival rate along with minimal signs of nerve agent toxicity. Recombinant PON1 pretreated animals exposed to sarin or soman prevented the reduction of blood O 2 saturation and pulse rate observed after nerve agent exposure. In addition, rePON1 pretreated animals showed significantly higher blood PON1, acetylcholinesterase (AChE), and butyrylcholinesterase activity after nerve agent exposure compared to the respective controls without treatments. AChE activity in different brain regions of rePON1 pretreated animals exposed to sarin or soman were also significantly higher than respective controls. The remaining activity of blood PON1, cholinesterases and brain AChE in PON1 pretreated animals after nerve agent exposure correlated with the survival rate. In summary, these data suggest that human rePON1 protects against sarin and soman exposure in guinea pigs.

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“…The enzyme PON-1 hydrolyzes the active metabolites, i.e., oxons of a number of organophosphate insecticides including diazoxan, dichlorvos, and chlorpyrifos oxon [64]. The catalytic efficiency of the enzyme appeared to determine the susceptibility to organophosphates, while the purified PON-1 itself was able to protect against toxicity induced by paraoxon or chlorpyrifos oxon in rodents [65][66][67]. There is an increasingly recognized role for PON-1 in a number of central nervous system diseases, including dementia [68], and autism [69].…”

Section: Rosmentioning

confidence: 99%

Grape Seed Extract Exerts an Anti-Apoptotic Effect and Attenuates the Decrease in Striatal Tyrosine Hydroxylase in Rotenone-Treated Mice

Abdel-Salam

El-Shamarka

Omara

2019

ROS

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The potential neuroprotective effect of grape seed extract (GSE) was evaluated in the rotenoneinduced Parkinson's disease in mice. Rotenone was administered at the dose of 1.5 mg/kg subcutaneously (sc) three times per week for 2 weeks alone or in combination with GSE at doses of 13.5 and 27 mg/kg, sc, daily. The control group received the vehicle. The brain levels of the lipid peroxidation product malondialdehyde (MDA), reduced glutathione (GSH), nitric oxide (nitrite), and paraoxonase-1 (PON-1) were determined. Histopathology, caspase-9 immunohistochemistry in different brain regions, and tyrosine hydroxylase immunoreactivity (TH-ir) in the substantia nigra were performed. Behavioral testing included rearing activity, locomotor activity, and stair test paradigms. Results indicated significantly increased lipid peroxidation and nitric oxide contents along with a significant decrease in GSH level and marked inhibition of PON-1 activity in the striatum and in the rest of the brain tissue in rotenone-treated mice. Rotenone caused significant decreases in rearing and locomotor activities and impaired motor strength. Treatment with GSE at 27 mg/kg resulted in decreased MDA and nitric oxide by 22.8%/17.9% and 38.5%/45.5%, respectively, in the striatum and the rest of the brain. GSH was increased by 20.8% and 26%, while PON-1 activity increased by 204% and 142.9% after GSE treatment in the striatum and in the rest of the brain tissue, respectively, compared with the corresponding rotenone control values. GSE given at 27 mg/kg almost completely corrected the decrease in motor activity and motor strength caused by rotenone. Neuronal degeneration and the increase in caspase-9 expression caused by rotenone in different brain regions as well as the loss of substantia nigra TH-ir were markedly reduced by GSE. These data indicate that GSE was effective in improving brain oxidative stress and in preventing the behavioral deficits and neurodegeneration induced by rotenone in the mouse brain. It is suggested that GSE might be useful as an adjunctive treatment in patients with Parkinson's disease.

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Study of paraoxonase-1 function on tissue damage of dichlorvos

Cited by 8 publications

References 8 publications

Novel Protective Effects of Brilliant Blue G in Acute Malathion Toxicity

Novel Protective Effects of Brilliant Blue G in Acute Malathion Toxicity

Recombinant paraoxonase 1 protects against sarin and soman toxicity following microinstillation inhalation exposure in guinea pigs

Grape Seed Extract Exerts an Anti-Apoptotic Effect and Attenuates the Decrease in Striatal Tyrosine Hydroxylase in Rotenone-Treated Mice

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