Di (2-ethylhexyl) phthalate induces cardiac disorders in BALB/c mice.
Cardiotoxicity
Di (2-ethylhexyl) phthalate
Genotoxicity
Lipid peroxidation
Oxidative stress
Phthalate
Journal
Environmental science and pollution research international
ISSN: 1614-7499
Titre abrégé: Environ Sci Pollut Res Int
Pays: Germany
ID NLM: 9441769
Informations de publication
Date de publication:
Mar 2019
Mar 2019
Historique:
received:
06
11
2018
accepted:
09
01
2019
pubmed:
20
1
2019
medline:
6
5
2019
entrez:
20
1
2019
Statut:
ppublish
Résumé
Because of the extensive use of phthalates for domestic, medical, and industrial applications, the evaluation of their toxic effects is of major concern to public health. The aim of the present study was to assess the propensity of di (2-ethylhexyl) phthalate (DEHP), one of the most used phthalates, to cause oxidative cardiac damage in mice. DEHP was administered intraperitoneally at doses of 5, 50, and 200 mg/kg body weight for 30 consecutive days in BALB/c mice. We assessed the effect of DEHP on cardiac injury using biochemical profile (such as aspartate aminotransferase (AST), alanine aminotransferase (ALT), lactate dehydrogenase (LDH), creatinine phosphokinase (CPK), total cholesterol (T-CHOL), triglyceride (TG), high-density lipoprotein cholesterol (HDL-C), and low-density lipoprotein cholesterol (LDL-C)), parameters related to myocardiac oxidative stress, such as malondialdehyde (MDA) level, protein carbonyl (PC) concentration, and DNA fragmentation. In addition, we evaluated antioxidant status; enzymatic (catalase (CAT) and superoxide dismutase (SOD) activities) and non-enzymatic (protein-bound sulfhydryl concentration (PSH)) antioxidants. Acetylcholinesterase (AChE) activity and histopathological changes were also assessed in heart mice treated with DEHP. Our results showed that DEHP induced an elevation of serum marker enzymes and perturbated the lipid profile. In addition, this phthalate increased lipid peroxidation, protein carbonyl levels, and DNA fragmentation in the heart in a dose-dependent manner. Antioxidant status was also perturbated by the increase of the CAT and SOD activities and the decrease of the protein-bound sulfhydryl concentration. AChE activity was also inhibited in the heart following the treatment with DEHP. These biochemical alterations were also confirmed by histopathological changes. Increased free radical production at various doses of DEHP would result in impairment of the redox status leading to an enhanced dose-dependent cardiotoxicity.
Identifiants
pubmed: 30659488
doi: 10.1007/s11356-019-04219-w
pii: 10.1007/s11356-019-04219-w
doi:
Substances chimiques
Antioxidants
0
Hazardous Substances
0
Phthalic Acids
0
Malondialdehyde
4Y8F71G49Q
phthalic acid
6O7F7IX66E
Diethylhexyl Phthalate
C42K0PH13C
Catalase
EC 1.11.1.6
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
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