BISPHENOL A DOSE- AND TIME-DEPENDENTLY INDUCES OXIDATIVE STRESS IN RAT LIVER MITOCHONDRIA EX VIVO

Objective: The probable toxic effects of bisphenol A (BPA) on different physiological functions have been reported in animal models. The role of BPA in mitochondrial oxidative stress has not been reported till date. The present study is aimed to elucidate dose- and time-dependent oxidative stress generation by BPA, respectively, in rat liver mitochondria in ex vivo model. Methods: The incubation mixture of BPA-treated groups containing mitochondria, 50 mM potassium phosphate buffer (pH 7.4), and different concentrations of BPA (20–160 μM/ml) (dissolved in 12% DMSO) in a final volume of 1.0 ml was incubated at 37°C in incubator for different time durations (30 min–2 h). Whereas, the incubation mixture of control group contained DMSO (12%), mitochondria and 50 mM potassium phosphatebuffer (pH 7.4).’ will be replaced by ‘Whereas, the incubation mixture of control group contained the same constituents except BPA. Result: We have observed significant decrease in mitochondrial intactness incubated with BPA in dose- and time-dependent manner under bright field and confocal microscopic study compared to control. Further, we have observed a decrease in mitochondrial reduced glutathione (GSH) content and increase in lipid peroxidation and protein carbonylation levels in dose- and time-dependent manner in BPA-exposed mitochondria. We have found a significant increase in the activity of Mn-superoxide dismutase and decrease in the activities of GSH peroxidase, GSH reductase, pyruvate dehydrogenase, and other three enzymes of Kreb’s cycle dose and time dependently in BPA-exposed mitochondria. The results indicate that exposure to BPA leads to decrease in intactness of mitochondria and increase in oxidative stress in mitochondria isolated from rat liver in a dose- and time-dependent manner. Conclusion: It can be concluded that the incubation of mitochondria isolated from rat liver with BPA, caused oxidative stress-mediated damages in mitochondria in both dose- and time-dependent manners.

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Gallic acid protects rat liver mitochondria ex vivo from bisphenol A induced oxidative stress mediated damages

Toxicology Reports ◽

10.1016/j.toxrep.2019.06.011 ◽

2019 ◽

Vol 6 ◽

pp. 578-589 ◽

Cited By ~ 9

Author(s):

Mousumi Dutta ◽

Goutam Paul

Keyword(s):

Oxidative Stress ◽

Bisphenol A ◽

Gallic Acid ◽

Rat Liver ◽

Ex Vivo ◽

Liver Mitochondria ◽

Rat Liver Mitochondria

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NF-κB and FosB mediate inflammation and oxidative stress in the blast lung injury of rats exposed to shock waves

Acta Biochimica et Biophysica Sinica ◽

10.1093/abbs/gmaa179 ◽

2021 ◽

Author(s):

Hong Wang ◽

Wenjuan Zhang ◽

Jinren Liu ◽

Junhong Gao ◽

Le Fang ◽

...

Keyword(s):

Oxidative Stress ◽

Lung Injury ◽

Shock Waves ◽

Time Dependent ◽

Inflammatory Factors ◽

Control Group ◽

Dependent Manner ◽

Total Antioxidant ◽

Blast Lung Injury ◽

And Oxidative Stress

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<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.

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Catalase Takes Part in Rat Liver Mitochondria Oxidative Stress Defense

Journal of Biological Chemistry ◽

10.1074/jbc.m701589200 ◽

2007 ◽

Vol 282 (33) ◽

pp. 24407-24415 ◽

Cited By ~ 140

Author(s):

Mauro Salvi ◽

Valentina Battaglia ◽

Anna Maria Brunati ◽

Nicoletta La Rocca ◽

Elena Tibaldi ◽

...

Keyword(s):

Oxidative Stress ◽

Rat Liver ◽

Liver Mitochondria ◽

Rat Liver Mitochondria ◽

Oxidative Stress Defense ◽

Stress Defense

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Time-dependence of inhibition of carnitine palmitoyltransferase I by malonyl-CoA in mitochondria isolated from livers of fed or starved rats. Evidence for transition of the enzyme between states of low and high affinity for malonyl-CoA

Biochemical Journal ◽

10.1042/bj2180379 ◽

1984 ◽

Vol 218 (2) ◽

pp. 379-386 ◽

Cited By ~ 21

Author(s):

V A Zammit

Keyword(s):

Rat Liver ◽

Initial Rate ◽

Liver Mitochondria ◽

Time Dependent ◽

Rat Liver Mitochondria ◽

High Affinity ◽

Malonyl Coa ◽

Rate Of Increase ◽

Cpt I ◽

Zero Time

The degree of inhibition of CPT I (carnitine palmitoyltransferase, EC 2.3.1.21) in isolated rat liver mitochondria by malonyl-CoA was studied by measuring the activity of the enzyme over a short period (15s) after exposure of the mitochondria to malonyl-CoA for different lengths of time. Inhibition of CPT I by malonyl-CoA was markedly time-dependent, and the increase occurred at the same rate in the presence or absence of palmitoyl-CoA (80 microM), and in the presence of carnitine, such that the time-course of acylcarnitine formation deviated markedly from linearity when CPT I activity was measured in the presence of malonyl-CoA over several minutes. The initial rate of increase in degree of inhibition with time was independent of malonyl-CoA concentration. CPT I in mitochondria from 48 h-starved rats had a lower degree of inhibition by malonyl-CoA at zero time, but was equally capable of being sensitized to malonyl-CoA, as judged by an initial rate of increase of inhibition identical with that of the enzyme in mitochondria from fed rats. Double-reciprocal plots for the degree of inhibition produced by different malonyl-CoA concentrations at zero time for the enzyme in mitochondria from fed or starved animals indicated that the enzyme in the latter mitochondria was predominantly in a state with low affinity for malonyl-CoA (concentration required to give 50% inhibition, I0.5 congruent to 10 microM), whereas that in mitochondria from fed rats displayed two distinct sets of affinities: low (congruent to 10 microM) and high (less than 0.3 microM). Plots for mitochondria after incubation for 0.5 or 1 min with malonyl-CoA indicated that the increased sensitivity observed with time was due to a gradual increase in the high-affinity state in both types of mitochondria. These results suggest that the sensitivity of CPT I in rat liver mitochondria in vitro had two components: (i) an instantaneous sensitivity inherent to the enzyme which depends on the nutritional state of the animal from which the mitochondria are isolated, and (ii) a slow, malonyl-CoA-induced, time-dependent increase in sensitivity. It is suggested that the rate of malonyl-CoA-induced sensitization of the enzyme to malonyl-CoA inhibition is limited by a slow first-order process, which occurs after the primary event of interaction of malonyl-CoA with the mitochondria.(ABSTRACT TRUNCATED AT 400 WORDS)

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Nitric oxide produced in rat liver mitochondria causes oxidative stress and impairment of respiration after transient hypoxia

The FASEB Journal ◽

10.1096/fj.02-1170com ◽

2003 ◽

Vol 17 (15) ◽

pp. 2194-2201 ◽

Cited By ~ 55

Author(s):

Lorenz Schild ◽

Thomas Reinheckel ◽

Michael Reiser ◽

Thomas F. W. Horn ◽

Gerald Wolf ◽

...

Keyword(s):

Oxidative Stress ◽

Nitric Oxide ◽

Rat Liver ◽

Liver Mitochondria ◽

Rat Liver Mitochondria

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Effect of graded corticosterone treatment on aging-related markers of oxidative stress in rat liver mitochondria

Biogerontology ◽

10.1007/s10522-006-9026-x ◽

2006 ◽

Vol 8 (1) ◽

pp. 1-11 ◽

Cited By ~ 24

Author(s):

Pilar Caro ◽

José Gómez ◽

Alberto Sanz ◽

Manel Portero-Otín ◽

Reinald Pamplona ◽

...

Keyword(s):

Oxidative Stress ◽

Rat Liver ◽

Liver Mitochondria ◽

Rat Liver Mitochondria ◽

Markers Of Oxidative Stress ◽

Corticosterone Treatment

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The effects of CeO2 nanoparticle (CeNPs) on oxidative stress biomarkers of rat liver mitochondria: In vitro study ‏

Nanoscience &Nanotechnology-Asia ◽

10.2174/2210681210666200206123523 ◽

2020 ◽

Vol 10 ◽

Author(s):

Mona Pourjafar ◽

Sara Malih ◽

Akram Ranjbar

Keyword(s):

Oxidative Stress ◽

Rat Liver ◽

Antioxidant Properties ◽

In Vitro Study ◽

Liver Mitochondria ◽

Rat Liver Mitochondria ◽

Oxidative Stress Biomarkers ◽

Beneficial Effects ◽

Stress Biomarkers

: In recent years, the applications of nanoparticles have received a great attention due to their industrial and biomedical applications, while their beneficial effects suffer from controversial results at clinical stages. In the current study, cytotoxicity of cerium oxide (CeNP) nanoparticles (100 nm) were evaluated using mitochondria derived from wistar rat's liver. Isolated mitochondria from rat’s liver were divided into 7 groups including group 1 as control and group 2 to 7 as treatment group with different doses of CeNP (5, 10, 50, 100, 250 and 500mg/ml, respectively), for 24,48 and 72 hours. After exposure, oxidative stress biomarkers such as total ‎antioxidant capacity (TAC), lipid peroxidation (LPO), total thiol groups (TTG), catalase activity (CAT) and mitochondrial viability, were determined in isolated rat liver mitochondria. Results have shown that CeNPs increase TAC, TTG, CAT, LPO and viability of mitochondria in various exposure times and confirm antioxidant properties of CeNPs in mithocondria while mitochondria is a main source for the generation of reactive oxygen species (ROS).

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