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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Vydáno v:Biological trace element research Ročník 199; číslo 3; s. 1052 - 1061
Hlavní autoři: Salau, Veronica F., Erukainure, Ochuko L., Islam, Md. Shahidul
Médium: Journal Article
Jazyk:angličtina
Vydáno: New York Springer US 01.03.2021
Springer Nature B.V
Témata:
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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Shrnutí: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.
Bibliografie:ObjectType-Article-1
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ISSN:0163-4984
1559-0720
1559-0720
DOI:10.1007/s12011-020-02227-3