Protective Effects of Onion Extract on Cadmium-Induced Oxidative Stress, Histological Damage, and Apoptosis in Rat Heart

Alpsoy, Şeref; Kanter, Mehmet; Aktaş, Cevat; Erboğa, Mustafa; Akyüz, Aydın; Akkoyun, Dursun Çayan; Oran, Mustafa

doi:10.1007/s12011-014-9968-9

Cited by 31 publications

(18 citation statements)

References 33 publications

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“…SOD is an antioxidant enzyme that catalyses the conversion of anion superoxide (O 2 • ) into oxygen (O 2 ) and H 2 O 2 and CAT completing detoxification process initiated by SOD. The lower activities of SOD and CAT found in diabetic rats is in agreement with the previous studies (Alpsoy et al, 2014;Jemai & Sayadi, 2015). This was probably due to the increment of antioxidant enzyme usage to compensate with the increased production of ROS.…”

Section: Effects Of Hpe On Oxidative Stress Status Of Thoracic Aortasupporting

confidence: 92%

Hibiscus sabdariffa Linn. improves the aortic damage in diabetic rats by acting as antioxidant

Zainalabidin¹,

Budin²,

Anuar³

et al. 2018

J App Pharm Sci

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Chronic hyperglycaemia produces excessive free radicals which could lead to diabetic complications. Hibiscus sabdariffa Linn. is proven to have high antioxidant and antihyperlipidemic properties. The aim of the study was to investigate the effects of H. sabdariffa polyphenol-rich extract (HPE) in the aorta of diabetic rats. Twenty-four male rats were randomly divided into three groups, i.e. non-diabetes mellitus (NDM), diabetes mellitus (DM) and diabetes mellitus with HPE (DM + HPE). HPE at 100 mg/kg or saline as control vehicle were administered daily through oral gavage for 28 days prior to sacrification and the aorta was isolated for further analysis. The glucose level in DM + HPE was significantly lower compared to DM, indicating its potential as an antidiabetic agent. Conversely, catalase (CAT), superoxide dismutase (SOD) activity and the level of glutathione (GSH) in DM + HPE were significantly higher than DM. The level of malondialdehyde (MDA) and protein carbonyl were significantly lower in DM + HPE than DM. Lipid profile analysis demonstrated a significant decrease in triglyceride, total cholesterol and LDL-C in DM + HPE compared to DM, however, HDL-C was significantly increased. Microscopic observation showed a disrupted morphology of the thoracic aorta in diabetic rats. HPE may exert protective effects by acting as an antidiabetic, antihyperlipidemic and antioxidant agent to the thoracic aorta in diabetic rats.

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Section: Effects Of Hpe On Oxidative Stress Status Of Thoracic Aortasupporting

confidence: 92%

Hibiscus sabdariffa Linn. improves the aortic damage in diabetic rats by acting as antioxidant

Zainalabidin¹,

Budin²,

Anuar³

et al. 2018

J App Pharm Sci

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“…Important Cd sources affecting human life are cigarette smoke, refined nutrients, water pipes, coffee, tea, products released by burning coal, shellfishes, fertilizers used, dyes and batteries containing Cd, and flue gases released in industrial production stages [7]. Occupational and environmental Cd exposure cause serious damages in the tissues like the placenta, kidney, liver, testis, heart, brain, and lungs [8][9][10][11][12][13][14][15]. Several investigations confirmed its transport across the placenta and accumulation in fetuses [16,17].…”

Section: Introductionmentioning

confidence: 99%

Effect of Cadmium on Trophoblast Cell Proliferation and Apoptosis in Different Gestation Periods of Rat Placenta

Erboğa

Kanter

2015

Biol Trace Elem Res

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In this study, we aimed to show how cadmium (Cd) affects the trophoblast proliferation and differentiation in the placenta and the apoptotic activity in different gestational days and, hence, its effects of placental development with immunohistochemical and TUNEL techniques. Experimental model of our study consisted of placental development of control and Cd groups on 15, 17, 19, and 21th days of the gestation. Female rats in Cd groups were subcutaneously administered a single dose of 0.5 mg Cd/kg/day dissolved in sodium chloride as 2 mL/kg Cd chloride until the day they sacrificed. Embryo and placenta of female rats were separately removed on 15, 17, 19, and 21th days of the gestation in which the placental development takes place and placentas were processed for microscopic examinations. In the placentas of the control group, all layers were observed to be formed on the 15th gestational day and thereafter a continuous growth was monitored. In the Cd group also all layers existed from the 15th gestational day. However, they were smaller in size than control groups. Frequency of proliferating cell nuclear antigen (PCNA)-positive cells was decreased and the number of apoptotic cells was increased in all the gestational days related to Cd. In conclusion, Cd administered during the pregnancy was observed to cause abnormal placental development by disrupting the normal structure of the placenta, inhibiting the proliferation of trophoblast and increasing the number of apoptotic trophoblast cells.

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“…36,37 Extensive studies have indicated that Cd exposure induced oxidative stress, histological damage, and cardiomyocyte apoptosis in the cardiac tissue of rats. 25 Therefore, it could be concluded that Cd induces cardiotoxicity and cell death along with myocardial ber necrosis in the cardiac tissue. In addition, numerous studies revealed that the exposure to Cd increased the ROS production with oxidative stress resulting in tissue damage in rats.…”

Section: Discussionmentioning

confidence: 99%

“…41 Furthermore, Cd exposure induced signicant histological changes, which led to myobrillar loss, oedema, vacuolization of cytoplasm, vitreous degeneration, inltration of dense focal inammatory cells and irregularity of myobrils in the cardiac tissues of chicken. 25 In another study, the mode of Cd-induced programmed necrosis in human endothelial cells along with DNA damage has been determined. 42 The results of the present study are consistent with those previously reported, which have proved that some genes (JNK, TNFa, RIPK1 and MLKL) related to necroptosis pathway remarkably increased as observed in the Cd + group in our experiments.…”

Section: Discussionmentioning

confidence: 99%

“…23,24 Further, it has been reported that Se reduces the Cd-induced oxidative stress and the histopathological damage in the rat heart. 25 We have previously demonstrated that Se could attenuate Cd-induced brain damage in chickens by regulating the iNOS-NO system. 26 In addition, the results obtained in our study suggested that Se has an ability to inhibit mitochondrial apoptotic pathway in the oxidative stress mediated kidney dysfunction caused by Cd.…”

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confidence: 98%

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Antagonistic effects of selenium against necroptosis injury via adiponectin-necrotic pathway induced by cadmium in heart of chicken

et al. 2017

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Cadmium (Cd) is one of the most toxic heavy metals having a destructive impact on various organ systems.For example, it induces oxidative stress in heart of chicken. Selenium (Se), in the form of selenoproteins, is known to protect tissues and organs against such heavy metal induced-damage. However, the precise cellular mechanism of the ameliorative role of Se in preventing Cd-induced toxicity in cardiac tissues remains unclear. The aim of this study is to investigate the role of Se in preventing Cd-induced toxicity in the chicken heart and assess the possible cytoprotective mechanism of Se. A total of 128 chickens were divided into four trial groups fed by a standard diet comprising Se, Se + , Cd + , and Se + + Cd + for 90 days.qPCR and western blotting were performed to observe the mRNA and protein expression of genes.Correlation analysis (PPI) and heat maps were used for further analysis. The results revealed that the exposure to Cd significantly increased (p < 0.05) the mRNA and protein levels of c-Jun N-terminal kinase (JNK), phosphorylated c-Jun N-terminal kinase (P-JNK), tumor necrosis factor a (TNFa), protein kinase superfamily protein 1 (RIPK1) and mixed lineage kinase domain like pseudokinase (MLKL) in the chicken. On the contrary, the mRNA and protein expression of peroxisome proliferator activated receptor alpha (PPARa), adiponectin (ADIPOQ), adiponectin receptor 1 (AdipoR1), adiponectin receptor 2 (AdipoR2), and adenosine monophosphate-activated protein kinase alpha 1 (AMPKa1) were significantly decreased in the Cd + group. Furthermore, the mRNA and protein expression levels of PPARa, adiponectin, adipoR1, adipoR2 and AMPK1 were increased (p < 0.05) significantly in the Se + group.However, the expression of JNK, TNFa and RIPK1 was significantly decreased as compared to that in the group provided with a normal standard diet. Notably, no significant increase in JNK, TNFa, RIPK1 and MLKL expression levels were observed in the chickens provided with a diet comprising Se + + Cd + , whereas the expression levels of PPARa, adiponectin, adipoR1, adipoR2 and AMPK1 were increased significantly as compared to those in the Cd + group. These results evidently indicated that Cd could induce severe myocardial damage by activating the necroptosis pathway, whereas Se could play an excellent potential role in preventing Cd-induced myocardial damage through activating adiponectin pathway.

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Protective Effects of Onion Extract on Cadmium-Induced Oxidative Stress, Histological Damage, and Apoptosis in Rat Heart

Cited by 31 publications

References 33 publications

Hibiscus sabdariffa Linn. improves the aortic damage in diabetic rats by acting as antioxidant

Hibiscus sabdariffa Linn. improves the aortic damage in diabetic rats by acting as antioxidant

Effect of Cadmium on Trophoblast Cell Proliferation and Apoptosis in Different Gestation Periods of Rat Placenta

Antagonistic effects of selenium against necroptosis injury via adiponectin-necrotic pathway induced by cadmium in heart of chicken

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