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Protective effect of quercetin against oxidative Stress and mitochondrial bioenergetic deficiency caused by lambda- cyhalothrin [electronic resource]

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Hamed, Nadia A

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Language: English Summary language: Arabic Description: P. 83-88Other title:

التأثير الوقائى للكيرسيتين ضد الاكسدة و نقص الطاقة البيولوجية فى الميتوكوندريا التى يسببها لامبادا سيهالوثرين [Added title page title]

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Alexandria science exchange journal, 2017 v. 38 (1) [electronic resource]:

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Full Text Article

In: Alexandria Science Exchange Journal 2017.v.38(1)Summary: Mitochondria are a convenient model to understand the oxidative damage induced by various xenobioticprooxidants. This study was designed to investigate (1) the possibility of lambda-cyhalothrin (LCT), a type II pyrethroid, to induce oxidative stress response in rabbit liver mitochondria in vitro and its effect on selected parameters and (2) the role of quercetin in alleviating the cytotoxic effects of LCT. Mitochondria were divided into two groups. The first group, mitochondria were incubated for 30 min at 37oC with different concentrations (0, 5, 10, 15 and 20uM) of LCT. In the second group, mitochondria were pre-incubated with (10µM) quercetin for 30 min and followed by LCT incubation for 30 min at 37oC. Following in vitro exposure, LCT caused a significant induction of oxidative damage in mitochondria at all tested concentrations as evidenced by increased superoxide dismutase (SOD) activity and reduced glutathione (GSH) level. However, a significant decrease in the activities of NADH dehydrogenase and ATP synthase (ATPase) was obtained. While the quercetin treated mitochondria showed significant enhancement in all tested parameters except GSH content, there was no significant change. Quercetin showed a significant protection against the cytotoxic effects induced by LCT on the studied parameters. In conclusion, antioxidant quercetin could be able to ameliorate LCT-induced oxidative stress by altering antioxidant defense system and recovered the bioenergetic activity of mitochondria.

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Item type	Current library	Call number	Status	Date due	Barcode
Articles	Main	ART ASEJ V38 No1 10 (Browse shelf(Opens below))	Available

Includes references.

Mitochondria are a convenient model to understand the oxidative damage induced by various xenobioticprooxidants. This study was designed to investigate (1) the possibility of lambda-cyhalothrin (LCT), a type II pyrethroid, to induce oxidative stress response in rabbit liver mitochondria in vitro and its effect on selected parameters and (2) the role of quercetin in alleviating the cytotoxic effects of LCT. Mitochondria were divided into two groups. The first group, mitochondria were incubated for 30 min at 37oC with different concentrations (0, 5, 10, 15 and 20uM) of LCT. In the second group, mitochondria were pre-incubated with (10µM) quercetin for 30 min and followed by LCT incubation for 30 min at 37oC. Following in vitro exposure, LCT caused a significant induction of oxidative damage in mitochondria at all tested concentrations as evidenced by increased superoxide dismutase (SOD) activity and reduced glutathione (GSH) level. However, a significant decrease in the activities of NADH dehydrogenase and ATP synthase (ATPase) was obtained. While the quercetin treated mitochondria showed significant enhancement in all tested parameters except GSH content, there was no significant change. Quercetin showed a significant protection against the cytotoxic effects induced by LCT on the studied parameters. In conclusion, antioxidant quercetin could be able to ameliorate LCT-induced oxidative stress by altering antioxidant defense system and recovered the bioenergetic activity of mitochondria.

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