Caffeic Acid Protects against Iron-Induced Cardiotoxicity by Suppressing Angiotensin-Converting Enzyme Activity and Modulating Lipid Spectrum, Gluconeogenesis and Nucleotide Hydrolyzing Enzyme Activities

The protective effects of caffeic acid on angiotensin-converting enzyme (ACE) and purinergic enzyme activities, as well as gluconeogenesis was investigated in iron-induced cardiotoxicity. Cardiotoxicity was induced in heart tissues harvested from healthy male SD rats by 0.1 mM FeSO 4 . Treatment was...

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Vydané v:	Biological trace element research Ročník 199; číslo 3; s. 1052 - 1061
Hlavní autori:	Salau, Veronica F., Erukainure, Ochuko L., Islam, Md. Shahidul
Médium:	Journal Article
Jazyk:	English
Vydavateľské údaje:	New York Springer US 01.03.2021 Springer Nature B.V
Predmet:	Acids Adenosine triphosphatase adenosinetriphosphatase Angiotensin Biochemistry Biomedical and Life Sciences Biotechnology Caffeic acid carboxylic ester hydrolases Cardiotoxicity Catalase Cholesterol Conversion Depletion Enzymatic activity Enzyme activity Enzymes Food irradiation fructose Gluconeogenesis glucose Glycogen Glycogen phosphorylase Glycogens Heart High density lipoprotein hydrolysis Iron Iron sulfates Life Sciences Lipase Lipids Low density lipoprotein males Malondialdehyde Nitric oxide Nucleotides Nutrition Oncology Peptidyl-dipeptidase A Phosphatase Phosphorylase Phosphorylases protective effect Tissue trace elements triacylglycerols Triglycerides Iron cardiotoxicity Purinergic activity Cardio-metabolism Caffeic acid
ISSN:	0163-4984, 1559-0720, 1559-0720
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Abstract	The protective effects of caffeic acid on angiotensin-converting enzyme (ACE) and purinergic enzyme activities, as well as gluconeogenesis was investigated in iron-induced cardiotoxicity. Cardiotoxicity was induced in heart tissues harvested from healthy male SD rats by 0.1 mM FeSO 4 . Treatment was carried out by co-incubating hearts tissues with caffeic acid and 0.1 mM FeSO 4 . Cardiotoxicity induction significantly ( p < 0.05) depleted GSH level, SOD, catalase, and ENTPDase activities, with concomitant elevation of the levels of malondialdehyde (MDA), nitric oxide, ACE, ATPase, glycogen phosphorylase, glucose 6-phosphatase, fructose 6-biphsophatase, and lipase activities. There was significant ( p < 0.05) reversion in these levels and activities on treatment with caffeic acid. Caffeic acid also caused depletion in cardiac levels of cholesterol, triglyceride, LDL-c, while elevating HDL-c level. Our results suggest the protective effect of caffeic acid against iron-mediated cardiotoxicity as indicated by its ability to suppress oxidative imbalance and ACE activity, while concomitantly modulating nucleotide hydrolysis and metabolic switch.
AbstractList	The protective effects of caffeic acid on angiotensin-converting enzyme (ACE) and purinergic enzyme activities, as well as gluconeogenesis was investigated in iron-induced cardiotoxicity. Cardiotoxicity was induced in heart tissues harvested from healthy male SD rats by 0.1 mM FeSO₄. Treatment was carried out by co-incubating hearts tissues with caffeic acid and 0.1 mM FeSO₄. Cardiotoxicity induction significantly (p < 0.05) depleted GSH level, SOD, catalase, and ENTPDase activities, with concomitant elevation of the levels of malondialdehyde (MDA), nitric oxide, ACE, ATPase, glycogen phosphorylase, glucose 6-phosphatase, fructose 6-biphsophatase, and lipase activities. There was significant (p < 0.05) reversion in these levels and activities on treatment with caffeic acid. Caffeic acid also caused depletion in cardiac levels of cholesterol, triglyceride, LDL-c, while elevating HDL-c level. Our results suggest the protective effect of caffeic acid against iron-mediated cardiotoxicity as indicated by its ability to suppress oxidative imbalance and ACE activity, while concomitantly modulating nucleotide hydrolysis and metabolic switch. The protective effects of caffeic acid on angiotensin-converting enzyme (ACE) and purinergic enzyme activities, as well as gluconeogenesis was investigated in iron-induced cardiotoxicity. Cardiotoxicity was induced in heart tissues harvested from healthy male SD rats by 0.1 mM FeSO . Treatment was carried out by co-incubating hearts tissues with caffeic acid and 0.1 mM FeSO . Cardiotoxicity induction significantly (p < 0.05) depleted GSH level, SOD, catalase, and ENTPDase activities, with concomitant elevation of the levels of malondialdehyde (MDA), nitric oxide, ACE, ATPase, glycogen phosphorylase, glucose 6-phosphatase, fructose 6-biphsophatase, and lipase activities. There was significant (p < 0.05) reversion in these levels and activities on treatment with caffeic acid. Caffeic acid also caused depletion in cardiac levels of cholesterol, triglyceride, LDL-c, while elevating HDL-c level. Our results suggest the protective effect of caffeic acid against iron-mediated cardiotoxicity as indicated by its ability to suppress oxidative imbalance and ACE activity, while concomitantly modulating nucleotide hydrolysis and metabolic switch. The protective effects of caffeic acid on angiotensin-converting enzyme (ACE) and purinergic enzyme activities, as well as gluconeogenesis was investigated in iron-induced cardiotoxicity. Cardiotoxicity was induced in heart tissues harvested from healthy male SD rats by 0.1 mM FeSO4. Treatment was carried out by co-incubating hearts tissues with caffeic acid and 0.1 mM FeSO4. Cardiotoxicity induction significantly (p < 0.05) depleted GSH level, SOD, catalase, and ENTPDase activities, with concomitant elevation of the levels of malondialdehyde (MDA), nitric oxide, ACE, ATPase, glycogen phosphorylase, glucose 6-phosphatase, fructose 6-biphsophatase, and lipase activities. There was significant (p < 0.05) reversion in these levels and activities on treatment with caffeic acid. Caffeic acid also caused depletion in cardiac levels of cholesterol, triglyceride, LDL-c, while elevating HDL-c level. Our results suggest the protective effect of caffeic acid against iron-mediated cardiotoxicity as indicated by its ability to suppress oxidative imbalance and ACE activity, while concomitantly modulating nucleotide hydrolysis and metabolic switch. The protective effects of caffeic acid on angiotensin-converting enzyme (ACE) and purinergic enzyme activities, as well as gluconeogenesis was investigated in iron-induced cardiotoxicity. Cardiotoxicity was induced in heart tissues harvested from healthy male SD rats by 0.1 mM FeSO4. Treatment was carried out by co-incubating hearts tissues with caffeic acid and 0.1 mM FeSO4. Cardiotoxicity induction significantly (p < 0.05) depleted GSH level, SOD, catalase, and ENTPDase activities, with concomitant elevation of the levels of malondialdehyde (MDA), nitric oxide, ACE, ATPase, glycogen phosphorylase, glucose 6-phosphatase, fructose 6-biphsophatase, and lipase activities. There was significant (p < 0.05) reversion in these levels and activities on treatment with caffeic acid. Caffeic acid also caused depletion in cardiac levels of cholesterol, triglyceride, LDL-c, while elevating HDL-c level. Our results suggest the protective effect of caffeic acid against iron-mediated cardiotoxicity as indicated by its ability to suppress oxidative imbalance and ACE activity, while concomitantly modulating nucleotide hydrolysis and metabolic switch.The protective effects of caffeic acid on angiotensin-converting enzyme (ACE) and purinergic enzyme activities, as well as gluconeogenesis was investigated in iron-induced cardiotoxicity. Cardiotoxicity was induced in heart tissues harvested from healthy male SD rats by 0.1 mM FeSO4. Treatment was carried out by co-incubating hearts tissues with caffeic acid and 0.1 mM FeSO4. Cardiotoxicity induction significantly (p < 0.05) depleted GSH level, SOD, catalase, and ENTPDase activities, with concomitant elevation of the levels of malondialdehyde (MDA), nitric oxide, ACE, ATPase, glycogen phosphorylase, glucose 6-phosphatase, fructose 6-biphsophatase, and lipase activities. There was significant (p < 0.05) reversion in these levels and activities on treatment with caffeic acid. Caffeic acid also caused depletion in cardiac levels of cholesterol, triglyceride, LDL-c, while elevating HDL-c level. Our results suggest the protective effect of caffeic acid against iron-mediated cardiotoxicity as indicated by its ability to suppress oxidative imbalance and ACE activity, while concomitantly modulating nucleotide hydrolysis and metabolic switch. The protective effects of caffeic acid on angiotensin-converting enzyme (ACE) and purinergic enzyme activities, as well as gluconeogenesis was investigated in iron-induced cardiotoxicity. Cardiotoxicity was induced in heart tissues harvested from healthy male SD rats by 0.1 mM FeSO 4 . Treatment was carried out by co-incubating hearts tissues with caffeic acid and 0.1 mM FeSO 4 . Cardiotoxicity induction significantly ( p < 0.05) depleted GSH level, SOD, catalase, and ENTPDase activities, with concomitant elevation of the levels of malondialdehyde (MDA), nitric oxide, ACE, ATPase, glycogen phosphorylase, glucose 6-phosphatase, fructose 6-biphsophatase, and lipase activities. There was significant ( p < 0.05) reversion in these levels and activities on treatment with caffeic acid. Caffeic acid also caused depletion in cardiac levels of cholesterol, triglyceride, LDL-c, while elevating HDL-c level. Our results suggest the protective effect of caffeic acid against iron-mediated cardiotoxicity as indicated by its ability to suppress oxidative imbalance and ACE activity, while concomitantly modulating nucleotide hydrolysis and metabolic switch.
Author	Islam, Md. Shahidul Salau, Veronica F. Erukainure, Ochuko L.
Author_xml	– sequence: 1 givenname: Veronica F. surname: Salau fullname: Salau, Veronica F. organization: Department of Biochemistry, School of Life Sciences, University of KwaZulu–Natal, Department of Biochemistry, Veritas University – sequence: 2 givenname: Ochuko L. surname: Erukainure fullname: Erukainure, Ochuko L. organization: Department of Biochemistry, School of Life Sciences, University of KwaZulu–Natal, Department of Pharmacology, University of the Free State – sequence: 3 givenname: Md. Shahidul orcidid: 0000-0003-0309-9491 surname: Islam fullname: Islam, Md. Shahidul email: islamd@ukzn.ac.za organization: Department of Biochemistry, School of Life Sciences, University of KwaZulu–Natal
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Snippet	The protective effects of caffeic acid on angiotensin-converting enzyme (ACE) and purinergic enzyme activities, as well as gluconeogenesis was investigated in... The protective effects of caffeic acid on angiotensin-converting enzyme (ACE) and purinergic enzyme activities, as well as gluconeogenesis was investigated in...
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SubjectTerms	Acids Adenosine triphosphatase adenosinetriphosphatase Angiotensin Biochemistry Biomedical and Life Sciences Biotechnology Caffeic acid carboxylic ester hydrolases Cardiotoxicity Catalase Cholesterol Conversion Depletion Enzymatic activity Enzyme activity Enzymes Food irradiation fructose Gluconeogenesis glucose Glycogen Glycogen phosphorylase Glycogens Heart High density lipoprotein hydrolysis Iron Iron sulfates Life Sciences Lipase Lipids Low density lipoprotein males Malondialdehyde Nitric oxide Nucleotides Nutrition Oncology Peptidyl-dipeptidase A Phosphatase Phosphorylase Phosphorylases protective effect Tissue trace elements triacylglycerols Triglycerides
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Title	Caffeic Acid Protects against Iron-Induced Cardiotoxicity by Suppressing Angiotensin-Converting Enzyme Activity and Modulating Lipid Spectrum, Gluconeogenesis and Nucleotide Hydrolyzing Enzyme Activities
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