Antioxidants do not prevent acrylonitrile-induced toxicity

Carrera, Marı́a Pilar; Antolı́n, Isaac; Martı́n, Vanesa; Sainz, Rosa M.; Mayo, Juan C.; Herrera, Federico; García-Santos, Guillermo; Rodrı́guez, Carmen

doi:10.1016/j.toxlet.2007.01.011

Cited by 12 publications

(9 citation statements)

References 43 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…This emphasized the important role of GSH in ACN toxicity. With the evidence that exposure to ACN causes GSH depletion in human astrocytes (Carrera et al, 2007;Enongene et al, 2000;Esmat et al, 2007;Jacob and Ahmed, 2003;Pu et al, 2009;Zhang et al, 2002), and that NAC, a GSH replenisher, can attenuate ACN-induced apoptosis in the present study, GSH depletion may be the main causation for ACN generation of oxidative stress, and hence apoptosis induction by ACN.…”

Section: Count Propidium Iodide (Pi)supporting

confidence: 52%

“…The ability to induce oxidative stress has been implicated for ACN toxicity in many studies (Enongene et al, 2000;Esmat et al, 2007;Jacob and Ahmed, 2003;Jiang et al, 1998;Kamendulis et al, 1999;Mahalakshmi et al, 2003;Pu et al, 2006). Although a contrary observation has been reported by Carrera et al (2007) as they showed that antioxidants (trolox, taurine, estradiol and melatonin) did not prevent ACN toxicity, NAC, a glutathione (GSH) precursor, provided protection from ACN cytoxicity in their experiment paradigm. This emphasized the important role of GSH in ACN toxicity.…”

Section: Count Propidium Iodide (Pi)mentioning

confidence: 92%

“…that an antioxidant, NAC, protects rat primary astrocytes (Carrera et al, 2007) and glial cells (Esmat et al, 2007) from ACN toxicity, suggesting the attribution of oxidative stress in ACN toxicity. The present study adds to previous reports demonstrating that ACN is capable of inducing apoptosis (Ghanayem et al, 1997;Mikhutkina et al, 2004) and generating ROS (Jacob and Ahmed, 2003;Kamendulis et al, 1999;Pu et al, 2009;Whysner et al, 1998;Zhang et al, 2002), and further identifying that the mechanism of ACN-induced cell death in human neuroblastoma SH-SY5Y cells is through induction of apoptosis involved in the generation of oxidative stress mediated Bax expression.…”

Section: Count Propidium Iodide (Pi)mentioning

confidence: 99%

“…It has been reported that treatment of ACN caused an increase in production of reactive oxygen species (ROS) (Jacob and Ahmed, 2003;Kamendulis et al, 1999;Pu et al, 2009;Whysner et al, 1998;Zhang et al, 2002). Additionally, ACN caused reduction of cellular antioxidants including glutathione, catalase and superoxide dismutase, as well as elevation of cellular enzymes involved in generation of oxidative stress such as lipid peroxidase and xanthine oxidase (Carrera et al, 2007;Esmat et al, 2007;Mahalakshmi et al, 2003;Zhang et al, 2002). These findings suggested that ACN induces oxidative stress via alteration of both generation of oxidative stress and cellular antioxidant capacity.…”

Section: Introductionmentioning

confidence: 97%

See 3 more Smart Citations

Acrylonitrile induced apoptosis via oxidative stress in neuroblastoma SH‐SY5Y cell

Watcharasit

Suntararuks

Visitnonthachai

et al. 2010

J of Applied Toxicology

View full text Add to dashboard Cite

Acrylonitrile (ACN) is a chemical that is widely used in the production of plastics, acrylic fibers, synthetic rubbers and resins. It has been reported that ACN can cause oxidative stress, a condition which is well recognized as an apoptotic initiator; however, information regarding ACN-induced apoptosis is limited. This present study investigated whether ACN induces apoptosis in human neuroblastoma SH-SY5Y cells, and whether its apoptotic induction involves oxidative stress. The results showed that ACN caused activation of caspase-3, a key enzyme involved in apoptosis, in a dose- and time-dependent manner. Detection of sub-G1 apoptotic cell death and apoptotic nuclear condensation revealed that ACN caused an increase in the number of apoptotic cells indicating ACN induces apoptosis in SH-SY5Y cells. ACN dose- and time-dependently increased the level of proapoptotic protein, Bax. Pretreatment with N-acetylcysteine (NAC), an antioxidant, attenuated caspase-3 activation by ACN, as evidenced by a reduction in proteolysis of PARP, a known caspase-3 substrate, as well as in the number of sub-G1 apoptotic cells. Moreover, induction of Bax by ACN was abolished by NAC. Taken together, the results indicate that ACN induces apoptosis in SH-SY5Y cells via a mechanism involving generation of oxidative stress-mediated Bax induction.

show abstract

Section: Count Propidium Iodide (Pi)supporting

confidence: 52%

Section: Count Propidium Iodide (Pi)mentioning

confidence: 92%

Section: Count Propidium Iodide (Pi)mentioning

confidence: 99%

Section: Introductionmentioning

confidence: 97%

See 2 more Smart Citations

Acrylonitrile induced apoptosis via oxidative stress in neuroblastoma SH‐SY5Y cell

Watcharasit

Suntararuks

Visitnonthachai

et al. 2010

J of Applied Toxicology

View full text Add to dashboard Cite

show abstract

“…AN, an EPA priority pollutant, is among the top 50 most widely used industrial compounds in the USA (Keith and Telliard, 1979). AN induced permanent toxicity (Carrera et al, 2007) and symptoms of chemical bronchitis/asthma (Mohan et al, 2006).…”

Section: Introductionmentioning

confidence: 99%

Optimization of acrylonitrile removal by activated carbon‐granular using response surface methodology

2009

View full text Add to dashboard Cite

A statistical Box-Behnken design of experiments was performed to evaluate the effects of individual operating variables and their interactions on the acrylonitrile (AN) removal of C 0 = 100 mg/L as fixed input parameter. The variables examined in this study included activated carbon-granular (AC) dosage, w, temperature, T, and time of contact, t. The significant variables and optimum conditions were identified (w = 4 g/L, T = 30 • C, and t = 120 min with AN uptake of 23.97 mg/g of AC) from statistical analysis of the experimental results using response surface methodology (RSM).Un plan des expériences statistiques de Box-Behnken aété conçu afin d'évaluer les effets des variables de fonctionnement individuelles et leurs interactions sur l'élimination de 100 mg/L d'acrylonitrile (AN) comme paramètre d'entrée fixe. Les variables examinées dans le cadre de cetté etude comprenaient le dosage de charbon granulaire activé (w), la température (T) et le temps de séjour (t). Les variables importantes et les conditions optimales ontété déterminées (et minimales avec une absorption de 23,97 mg/g d'AN)à partir de l'analyse statistique des résultats expérimentaux au moyen de la méthodologie de la surface de réponse (MSR).

show abstract

Glutathione-Dependent Detoxification Processes in Astrocytes

et al. 2014

View full text Add to dashboard Cite

Astrocytes have a pivotal role in brain as partners of neurons in homeostatic and metabolic processes. Astrocytes also protect other types of brain cells against the toxicity of reactive oxygen species and are considered as first line of defence against the toxic potential of xenobiotics. A key component in many of the astrocytic detoxification processes is the tripeptide glutathione (GSH) which serves as electron donor in the GSH peroxidase-catalyzed reduction of peroxides. In addition, GSH is substrate in the detoxification of xenobiotics and endogenous compounds by GSH-S-transferases which generate GSH conjugates that are efficiently exported from the cells by multidrug resistance proteins. Moreover, GSH reacts with the reactive endogenous carbonyls methylglyoxal and formaldehyde to intermediates which are substrates of detoxifying enzymes. In this article we will review the current knowledge on the GSH metabolism of astrocytes with a special emphasis on GSH-dependent detoxification processes.

show abstract

Antioxidants do not prevent acrylonitrile-induced toxicity

Cited by 12 publications

References 43 publications

Acrylonitrile induced apoptosis via oxidative stress in neuroblastoma SH‐SY5Y cell

Acrylonitrile induced apoptosis via oxidative stress in neuroblastoma SH‐SY5Y cell

Optimization of acrylonitrile removal by activated carbon‐granular using response surface methodology

Glutathione-Dependent Detoxification Processes in Astrocytes

Contact Info

Product

Resources

About