scholarly journals Renal effects of deltamethrin induced intoxication in Carassius auratus gibelio (Pisces cyprinidae)

2007 ◽  
Vol 23 (5-6-2) ◽  
pp. 399-404 ◽  
Author(s):  
D. Costin ◽  
A. Staicu ◽  
R. Huculeci ◽  
G. Stoian ◽  
M. Costache ◽  
...  

Freshwater goldfish Carassius auratus gibelio were exposed to 2?g/l delthametrin for one, 2, 3, 7 and 14 days. Activities of kidney catalase (EC 1.11.1.6), glutathione reductase (EC 1.6.4.2) and glutathione-Stransferase (EC 2.5.1.18) were affected in a time-dependent manner by the pesticide exposure compared to controls. The results indicate that C. auratus gibelio kidney resisted to oxidative stress by antioxidant mechanisms and developed an adaptative response.

2016 ◽  
Vol 58 ◽  
pp. 11-15 ◽  
Author(s):  
K.P. Asifa ◽  
K.C. Chitra

The present study was designed to evaluate the effects of nonylphenol in the pro-oxidant/ antioxidant system in ovary of the cichlid fish Etroplus maculatus. Fishes were exposed at two sublethal concentrations (one-fifth and one-tenth of LC50) of nonylphenol for 24, 72 and 96 h maintaining control groups. The oxidative stress indices as the activities of antioxidant enzymes, superoxide dismutase, catalase, glutathione reductase along with the levels of hydrogen peroxide generation and lipid peroxidation were monitored in concentration-and time-dependent manner. Activity of superoxide dismutase significantly (P<0.05) increased at both concentrations in time-dependent manner. Meanwhile the activities of catalase and glutathione reductase significantly (P<0.05) decreased after 72 and 96 h of nonylphenol treatment. The levels of hydrogen peroxide generation and lipid peroxidation increased in all treatment groups when compared to controls. The present results demonstrated that the induction of oxidative stress in ovary of fish by the generation of lipid peroxidation could be due to the exposure of environmental contaminant, nonylphenol. Therefore, the observed oxidative stress in ovary can be indicated as a mechanism of toxicity in the fish exposed to nonylphenol.


Author(s):  
Hong Wang ◽  
Wenjuan Zhang ◽  
Jinren Liu ◽  
Junhong Gao ◽  
Le Fang ◽  
...  

Abstract Blast lung injury (BLI) is the major cause of death in explosion-derived shock waves; however, the mechanisms of BLI are not well understood. To identify the time-dependent manner of BLI, a model of lung injury of rats induced by shock waves was established by a fuel air explosive. The model was evaluated by hematoxylin and eosin staining and pathological score. The inflammation and oxidative stress of lung injury were also investigated. The pathological scores of rats’ lung injury at 2 h, 24 h, 3 days, and 7 days post-blast were 9.75±2.96, 13.00±1.85, 8.50±1.51, and 4.00±1.41, respectively, which were significantly increased compared with those in the control group (1.13±0.64; P&lt;0.05). The respiratory frequency and pause were increased significantly, while minute expiratory volume, inspiratory time, and inspiratory peak flow rate were decreased in a time-dependent manner at 2 and 24 h post-blast compared with those in the control group. In addition, the expressions of inflammatory factors such as interleukin (IL)-6, IL-8, FosB, and NF-κB were increased significantly at 2 h and peaked at 24 h, which gradually decreased after 3 days and returned to normal in 2 weeks. The levels of total antioxidant capacity, total superoxide dismutase, and glutathione peroxidase were significantly decreased 24 h after the shock wave blast. Conversely, the malondialdehyde level reached the peak at 24 h. These results indicated that inflammatory and oxidative stress induced by shock waves changed significantly in a time-dependent manner, which may be the important factors and novel therapeutic targets for the treatment of BLI.


Toxins ◽  
2021 ◽  
Vol 13 (11) ◽  
pp. 787
Author(s):  
Enrique García-Pérez ◽  
Dojin Ryu ◽  
Hwa-Young Kim ◽  
Hae Dun Kim ◽  
Hyun Jung Lee

Ochratoxin A (OTA) is a mycotoxin that is potentially carcinogenic to humans. Although its mechanism remains unclear, oxidative stress has been recognized as a plausible cause for the potent renal carcinogenicity observed in experimental animals. The effect of OTA on oxidative stress parameters in two cell lines of LLC-PK1 and HK-2 derived from the kidneys of pig and human, respectively, were investigated and compared. We found that the cytotoxicity of OTA on LLC-PK1 and HK-2 cells was dose- and time-dependent in both cell lines. Furthermore, increased intracellular reactive oxygen species (ROS) induced by OTA in both cell lines were observed in a time-dependent manner. Glutathione (GSH) was depleted by OTA at >48 h in HK-2 but not in LLC-PK1 cells. While the mRNA levels of glucose-6-phosphate dehydrogenase (G6PD) and glutathione peroxidase 1 (GPX1) in LLC-PK1 were down-regulated by 0.67- and 0.66-fold, respectively, those of catalase (CAT), glutathione reductase (GSR), and superoxide dismutase 1 (SOD) in HK-2 were up-regulated by 2.20-, 2.24-, and 2.75-fold, respectively, after 72 h exposure to OTA. Based on these results, we conclude that HK-2 cells are more sensitive to OTA-mediated toxicity than LLC-PK1, and OTA can cause a significant oxidative stress in HK-2 as indicated by changes in the parameter evaluated.


2011 ◽  
Vol 38 (3) ◽  
pp. 769-775 ◽  
Author(s):  
WeiNa Xu ◽  
WenBin Liu ◽  
KangLe Lu ◽  
YangYang Jiang ◽  
GuiFeng Li

2018 ◽  
Vol 2 ◽  
pp. 239784731879485 ◽  
Author(s):  
OG Aztatzi-Aguilar ◽  
A Valdés-Arzate ◽  
Y Debray-García ◽  
ES Calderón-Aranda ◽  
M Uribe-Ramirez ◽  
...  

Exposure to particulate matter (PM) has been implicated in oxidative stress (OxS) and inflammation as underlying mechanisms of lung damage and cardiovascular alterations. PM is a chemical mixture that can be subdivided according to their aerodynamic size into coarse (CP), fine (FP), and ultrafine (UFP) particulates. We investigated, in a rat model, the induction of OxS (protein oxidation and antioxidant response), carcinogen-DNA adduct formation, and inflammatory mediators in lung in response to different airborne particulate fractions, CP, FP, and UFP, after an acute and subchronic exposure. In addition, OxS was evaluated in the aorta to assess the effects beyond the lungs. Exposure to CP, FP, and UFP induced time- and size-dependent lung protein oxidation and DNA adduct formation. After acute and subchronic exposure, nuclear factor erythroid-2 (Nrf2) activation was observed in the lung, by electrophoretic mobility shift assay, and the induction of mRNA antioxidant enzymes in the FP and UFP groups, but not in the CP. Cytokine concentration of interleukin 1β, interleukin 6, and macrophage inflammatory protein-2 was significantly increased in bronchoalveolar lavage fluid after acute exposure to FP and UFP. Activation of Nrf2 and expression of mRNA antioxidant enzymes were observed only after the subchronic exposure to FP and UFP in the aorta. Our results indicate that FP and UFP were mainly accountable for the oxidant toxic effects in the lung; OxS is spread from the lung to the cardiovascular system. We conclude that the biological mechanisms associated with transient OxS and inflammation are particle size and time-dependent exposure resulting in acute lung injury, which later reaches the vascular system.


Chemosphere ◽  
2011 ◽  
Vol 85 (6) ◽  
pp. 983-989 ◽  
Author(s):  
Olha I. Kubrak ◽  
Viktor V. Husak ◽  
Bohdana M. Rovenko ◽  
Janet M. Storey ◽  
Kenneth B. Storey ◽  
...  

Author(s):  
Michael W. Country ◽  
Michael G. Jonz

Neurons of the retina require oxygen to survive. In hypoxia, neuronal ATP production is impaired, ATP-dependent ion pumping is reduced, transmembrane ion gradients are dysregulated, and [Ca2+]i increases enough to trigger excitotoxic cell death. Central neurons of the common goldfish (Carassius auratus) are hypoxia-tolerant, but little is known about how goldfish retinas withstand hypoxia. To study the cellular mechanisms of hypoxia tolerance, we isolated retinal interneurons (horizontal cells; HCs), and measured intracellular Ca2+ concentration ([Ca2+]i) with Fura-2. Goldfish HCs maintained [Ca2+]i throughout 1 h of hypoxia, whereas [Ca2+]i increased irreversibly in HCs of the hypoxia-sensitive rainbow trout (Oncorhynchus mykiss) with just 20 min of hypoxia. Our results suggest mitochondrial ATP-dependent K+ channels (mKATP) are necessary to stabilize [Ca2+]i throughout hypoxia. In goldfish HCs, [Ca2+]i increased when mKATP was blocked with glibenclamide or 5-HD, whereas an mKATP agonist (diazoxide) prevented [Ca2+]i from increasing in hypoxia in trout HCs. We showed that hypoxia protects goldfish HCs via mKATP channels. Glycolytic inhibition with 2-deoxyglucose increased [Ca2+]i, which was rescued by hypoxia in an mKATP-dependent manner. We found no evidence of plasmalemmal KATP channels in patch-clamp experiments. Instead, we confirmed the involvement of KATP in mitochondria with TMRE imaging, as hypoxia rapidly (&lt;5 min) depolarized mitochondria in an mKATP-sensitive manner. We conclude that mKATP channels initiate a neuroprotective pathway in goldfish HCs to maintain [Ca2+]i and avoid excitotoxicity in hypoxia. This model provides novel insight into the cellular mechanisms of hypoxia tolerance in the retina.


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