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Arachidonic Acid Metabolism

The Experts below are selected from a list of 159 Experts worldwide ranked by ideXlab platform

Ayman O S Elkadi – 1st expert on this subject based on the ideXlab platform

  • acute doxorubicin toxicity differentially alters cytochrome p450 expression and Arachidonic Acid Metabolism in rat kidney and liver
    Drug Metabolism and Disposition, 2011
    Co-Authors: Beshay N M Zordoky, Anwar Anwarmohamed, Mona E Aboutabl, Ayman O S Elkadi

    Abstract:

    The use of doxorubicin (DOX) is limited by significant cardiotoxicity, nephrotoxicity, and hepatotoxicity. We have previously shown that DOX cardiotoxicity induces several cardiac cytochrome P450 (P450) enzymes with subsequent alteration in P450-mediated Arachidonic Acid Metabolism. Therefore, in the current study, we investigated the effect of acute DOX toxicity on P450 expression and Arachidonic Acid Metabolism in the kidney and liver of male Sprague-Dawley rats. Acute DOX toxicity was induced by a single intraperitoneal injection (15 mg/kg) of the drug. After 6 and 24 h, the kidneys and livers were harvested, and several P450 gene and protein expressions were determined by real-time polymerase chain reaction and Western blot analyses, respectively. Kidney and liver microsomal protein from control or DOX-treated rats was incubated with Arachidonic Acid, and its metabolites were determined by liquid chromatography-electron spray ionization-mass spectrometry. Our results showed that acute DOX toxicity caused an induction of CYP1B1 and CYP4A enzymes and an inhibition of CYP2B1 and CYP2C11 in both the kidney and liver. CYP2E1 was induced and soluble epoxide hydrolase (sEH) was inhibited in the kidney only. In addition, DOX toxicity caused a significant increase in epoxyeicosatrienoic Acids formation in the kidney and a significant increase in 20-hydroxyeicosatetraenoic Acid formation in both the kidney and the liver. In conclusion, acute DOX toxicity alters the expression of several P450 and sEH enzymes in an organ-specific manner. These changes can be attributed to DOX-induced inflammation and resulted in altered P450-mediated Arachidonic Acid Metabolism.

Beshay N M Zordoky – 2nd expert on this subject based on the ideXlab platform

  • acute doxorubicin toxicity differentially alters cytochrome p450 expression and Arachidonic Acid Metabolism in rat kidney and liver
    Drug Metabolism and Disposition, 2011
    Co-Authors: Beshay N M Zordoky, Anwar Anwarmohamed, Mona E Aboutabl, Ayman O S Elkadi

    Abstract:

    The use of doxorubicin (DOX) is limited by significant cardiotoxicity, nephrotoxicity, and hepatotoxicity. We have previously shown that DOX cardiotoxicity induces several cardiac cytochrome P450 (P450) enzymes with subsequent alteration in P450-mediated Arachidonic Acid Metabolism. Therefore, in the current study, we investigated the effect of acute DOX toxicity on P450 expression and Arachidonic Acid Metabolism in the kidney and liver of male Sprague-Dawley rats. Acute DOX toxicity was induced by a single intraperitoneal injection (15 mg/kg) of the drug. After 6 and 24 h, the kidneys and livers were harvested, and several P450 gene and protein expressions were determined by real-time polymerase chain reaction and Western blot analyses, respectively. Kidney and liver microsomal protein from control or DOX-treated rats was incubated with Arachidonic Acid, and its metabolites were determined by liquid chromatography-electron spray ionization-mass spectrometry. Our results showed that acute DOX toxicity caused an induction of CYP1B1 and CYP4A enzymes and an inhibition of CYP2B1 and CYP2C11 in both the kidney and liver. CYP2E1 was induced and soluble epoxide hydrolase (sEH) was inhibited in the kidney only. In addition, DOX toxicity caused a significant increase in epoxyeicosatrienoic Acids formation in the kidney and a significant increase in 20-hydroxyeicosatetraenoic Acid formation in both the kidney and the liver. In conclusion, acute DOX toxicity alters the expression of several P450 and sEH enzymes in an organ-specific manner. These changes can be attributed to DOX-induced inflammation and resulted in altered P450-mediated Arachidonic Acid Metabolism.

  • Acute Doxorubicin Toxicity Differentially Alters Cytochrome P450 Expression and Arachidonic Acid Metabolism in Rat Kidney and Liver
    Drug Metabolism and Disposition, 2011
    Co-Authors: Beshay N M Zordoky, Mona E Aboutabl, Anwar Anwar-mohamed, Ayman O.s. El-kadi

    Abstract:

    The use of doxorubicin (DOX) is limited by significant cardiotoxicity, nephrotoxicity, and hepatotoxicity. We have previously shown that DOX cardiotoxicity induces several cardiac cytochrome P450 (P450) enzymes with subsequent alteration in P450-mediated Arachidonic Acid Metabolism. Therefore, in the current study, we investigated the effect of acute DOX toxicity on P450 expression and Arachidonic Acid Metabolism in the kidney and liver of male Sprague Dawley rats. Acute DOX toxicity was induced by a single intraperitoneal injection of 15 mg/kg of the drug. After 6 and 24 h, the kidneys and livers were harvested and the expression of several P450 gene and protein expressions were determined by real time-PCR and Western blot analyses, respectively. Kidney and liver microsomal protein from control or DOX treated rats was incubated with Arachidonic Acid, and its metabolites were determined by liquid chromatography-electron spray ionization-mass spectrometry. Our results showed that acute DOX toxicity caused an induction of CYP1B1 and CYP4A enzymes and an inhibition of CYP2B1 and CYP2C11 in both the kidney and liver. CYP2E1 was induced and soluble epoxide hydrolase (sEH) was inhibited in the kidney only. In addition, DOX toxicity caused a significant increase in the epoxyeicosatrienoic Acids formation in the kidney and a significant increase in 20-hydroxyeicosatetraenoic Acid formation in both the kidney and the liver. In conclusion, acute DOX toxicity alters the expression of several P450 and sEH enzymes in an organ-specific manner. These changes can be attributed to DOX-induced inflammation and resulted in altered P450-mediated Arachidonic Acid Metabolism.

Mona E Aboutabl – 3rd expert on this subject based on the ideXlab platform

  • acute doxorubicin toxicity differentially alters cytochrome p450 expression and Arachidonic Acid Metabolism in rat kidney and liver
    Drug Metabolism and Disposition, 2011
    Co-Authors: Beshay N M Zordoky, Anwar Anwarmohamed, Mona E Aboutabl, Ayman O S Elkadi

    Abstract:

    The use of doxorubicin (DOX) is limited by significant cardiotoxicity, nephrotoxicity, and hepatotoxicity. We have previously shown that DOX cardiotoxicity induces several cardiac cytochrome P450 (P450) enzymes with subsequent alteration in P450-mediated Arachidonic Acid Metabolism. Therefore, in the current study, we investigated the effect of acute DOX toxicity on P450 expression and Arachidonic Acid Metabolism in the kidney and liver of male Sprague-Dawley rats. Acute DOX toxicity was induced by a single intraperitoneal injection (15 mg/kg) of the drug. After 6 and 24 h, the kidneys and livers were harvested, and several P450 gene and protein expressions were determined by real-time polymerase chain reaction and Western blot analyses, respectively. Kidney and liver microsomal protein from control or DOX-treated rats was incubated with Arachidonic Acid, and its metabolites were determined by liquid chromatography-electron spray ionization-mass spectrometry. Our results showed that acute DOX toxicity caused an induction of CYP1B1 and CYP4A enzymes and an inhibition of CYP2B1 and CYP2C11 in both the kidney and liver. CYP2E1 was induced and soluble epoxide hydrolase (sEH) was inhibited in the kidney only. In addition, DOX toxicity caused a significant increase in epoxyeicosatrienoic Acids formation in the kidney and a significant increase in 20-hydroxyeicosatetraenoic Acid formation in both the kidney and the liver. In conclusion, acute DOX toxicity alters the expression of several P450 and sEH enzymes in an organ-specific manner. These changes can be attributed to DOX-induced inflammation and resulted in altered P450-mediated Arachidonic Acid Metabolism.

  • Acute Doxorubicin Toxicity Differentially Alters Cytochrome P450 Expression and Arachidonic Acid Metabolism in Rat Kidney and Liver
    Drug Metabolism and Disposition, 2011
    Co-Authors: Beshay N M Zordoky, Mona E Aboutabl, Anwar Anwar-mohamed, Ayman O.s. El-kadi

    Abstract:

    The use of doxorubicin (DOX) is limited by significant cardiotoxicity, nephrotoxicity, and hepatotoxicity. We have previously shown that DOX cardiotoxicity induces several cardiac cytochrome P450 (P450) enzymes with subsequent alteration in P450-mediated Arachidonic Acid Metabolism. Therefore, in the current study, we investigated the effect of acute DOX toxicity on P450 expression and Arachidonic Acid Metabolism in the kidney and liver of male Sprague Dawley rats. Acute DOX toxicity was induced by a single intraperitoneal injection of 15 mg/kg of the drug. After 6 and 24 h, the kidneys and livers were harvested and the expression of several P450 gene and protein expressions were determined by real time-PCR and Western blot analyses, respectively. Kidney and liver microsomal protein from control or DOX treated rats was incubated with Arachidonic Acid, and its metabolites were determined by liquid chromatography-electron spray ionization-mass spectrometry. Our results showed that acute DOX toxicity caused an induction of CYP1B1 and CYP4A enzymes and an inhibition of CYP2B1 and CYP2C11 in both the kidney and liver. CYP2E1 was induced and soluble epoxide hydrolase (sEH) was inhibited in the kidney only. In addition, DOX toxicity caused a significant increase in the epoxyeicosatrienoic Acids formation in the kidney and a significant increase in 20-hydroxyeicosatetraenoic Acid formation in both the kidney and the liver. In conclusion, acute DOX toxicity alters the expression of several P450 and sEH enzymes in an organ-specific manner. These changes can be attributed to DOX-induced inflammation and resulted in altered P450-mediated Arachidonic Acid Metabolism.