Effects of cod liver oil on tissue antioxidant pathways in normal and streptozotocin‐diabetic rats

Hünkar, Tuǧba; Aktan, Fügen; Ceylan, Aslı F.; Karasu, Çi̇men

doi:10.1002/cbf.977

Cited by 77 publications

(63 citation statements)

References 34 publications

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“…All these effects were blocked by cod liver oil. Of note, it has been reported previously that cod liver oil reduced oxidative stress and augmented the antioxidant activity in other animal models that involve oxidative stress like streptozotocininduced diabetes in rats (Hunkar et al, 2002) and daunomycin-induced nephropathy in mice (Ohtake et al, 2002). Moreover, dietary supplementation with cod liver oil inactivates circulating neutrophils and plasma lipoperoxides (Guarnieri et al, 1991).…”

Section: Discussionmentioning

confidence: 90%

Hepatoprotective effects of cod liver oil against sodium nitrite toxicity in rats

Salama

Abbas

Darweish³

et al. 2013

Pharmaceutical Biology

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Context: Exposure to high levels of nitrites for a prolonged time have adverse health effects on several organs especially the liver due to oxidative properties. Meanwhile, cod liver oil has been reported to ameliorate organ dysfunction in animal models that involve oxidative stress. Objective: Examine the impact of dietary cod liver oil on sodium nitrite-induced liver damage. Materials and methods: Thirty-two adult male Sprague-Dawely rats were daily treated with sodium nitrite (80 mg/kg) in presence or absence of cod liver oil (5 ml/kg). Morphological changes were assessed in liver sections. Oxidative stress and antioxidant markers were measured in serum and liver homogenates. Liver samples were used for measurements of MCP-1, DNA fragmentation and mitochondrial function. Results: The hepatoprotective effect of cod liver oil was proved by significant reduction of elevated liver enzymes and normal appearance of hepatocytes. Cod liver oil significantly reduced hepatic malondialdehyde, hydrogen peroxide and superoxide anion (224.3 AE 18.9 nmol/g, 59.3 AE 5.1 and 62.5 AE 5.1 mmol/g, respectively) compared with sodium nitrite (332.5 AE 25.5 nmol/g, 83.1 AE 8.1 and 93.9 AE 6.5 mmol/g, respectively). Cod liver oil restored hepatic cytochrome c oxidase activity after 38% reduction by sodium nitrite. Furthermore, cod liver oil significantly reduced hepatic MCP-1 (79.8 pg/mg) and DNA fragmentation (13.8%) compared with sodium nitrite (168.7 pg/mg and 41.3%, respectively). Discussion and conclusion: Cod liver oil ameliorates sodium nitrite induced hepatic impairment through several mechanisms including attenuation of oxidative stress, blocking MCP-1, reactivation of mitochondrial function and reduction of DNA fragmentation.

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Section: Discussionmentioning

confidence: 90%

Hepatoprotective effects of cod liver oil against sodium nitrite toxicity in rats

Salama

Abbas

Darweish³

et al. 2013

Pharmaceutical Biology

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“…However, several reports have shown the beneficial effects of fish oils containing n-3 polyunsaturated fatty acids (PUFAs) like eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) in the protection against lipid peroxidation in rat and human beings with diabetes. 15,16 Owing to these beneficial effects of n-3 PUFA, we tested the hypothesis whether EPA and DHA are implicated in prevention and protection against free radical production or oxidative stress associated with lipid peroxidation in diabetes. To our knowledge, no studies have directly investigated the role of EPA and DHA in lipid metabolism and oxidative stress in macrosomia.…”

Section: Introductionmentioning

confidence: 99%

N-3 Fatty acids modulate antioxidant status in diabetic rats and their macrosomic offspring

et al. 2006

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Objective: We investigated the role of dietary n-3 polyunsaturated fatty acids (n-3 PUFA) in the modulation of total antioxidant status in streptozotocin (STZ)-induced diabetic rats and their macrosomic offspring. Design: Female wistar rats, fed on control diet or n-3 PUFA diet, were rendered diabetic by administration of five mild doses of STZ on day 5 and were killed on days 12 and 21 of gestation. The macrosomic (MAC) pups were killed at the age of 60 and 90 days. Measurements: Lipid peroxidation was measured as the concentrations of plasma thiobarbituric acid reactive substances (TBARS), and the total antioxidant status was determined by measuring (i) plasma oxygen radical absorbance capacity (ORAC), (ii) plasma vitamin A, E and C concentrations, and (iii) antioxidant enzymes activities in erythrocytes. The plasma lipid concentrations and fatty acid composition were also determined. Results: Diabetes increased plasma triglyceride and cholesterol concentrations, whereas macrosomia was associated with enhanced plasma cholesterol and triglyceride levels, which diminished by feeding n-3 PUFA diet. N-3 PUFA diet also reduced increased plasma TBARS and corrected the decreased ORAC values in diabetic rats and their macrosomic offspring. EPAX diet increased the diminished vitamin A levels in diabetic mothers and vitamin C concentrations in macrosomic pups. Also, this diet improved the decreased erythrocyte superoxide dismutase and glutathione peroxidase activities in diabetic and macrosomic animals. Conclusion: Diabetes and macrosomia were associated with altered lipid metabolism, antioxidant enzyme activities and vitamin concentrations. N-3 PUFA diet improved hyperlipidemia and restored antioxidant status in diabetic dams and MAC offspring.

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“…The level of MDA, an end-product of LPO, signifi cantly increased in the liver of the untreated diabetic rats. Thus, increased MDA level in diabetes mellitus suggests that hyperglycaemia induces peroxidative reactions in lipids (42). Besides, it has been reported that diabetes increased oxidative stress in many organs, especially in the liver (29).…”

Section: Discussionmentioning

confidence: 95%

The effects of caffeic acid phenethyl ester on streptozotocin-induced diabetic liver injury

Taşlıdere¹,

Gül²,

Elbe³

et al. 2016

BLL

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The aim of the present study was to clarify the role of oxidative stress in streptozotocin induced liver injury and the possible protective effect of caffeic acid phenethyl ester (CAPE) using histological and biochemical parameters. 32 male Wistar rats were divided into 4 groups as follows: Group 1: Control animals, Group 2: Control animals given CAPE Group 3: STZ-induced diabetic animals (DM group), Group 4: STZ-induced diabetic rats given CAPE (DM+CAPE group). All the injections started on the same day of single-dose STZ injection and continued for 20 days. At the end of this period, livers were removed and processed for routine histological procedures. Biochemical parameters and morphological changes were examined. In DM group, blood glucose levels were signifi cantly increased compared with the control group. Signifi cant increases in tissue malondialdehyde (MDA) level and decreases in superoxide dismutase (SOD) and total glutathione (GSH) activities were detected in DM group. Administration of CAPE signifi cantly reduced these values. STZ-induced histopathological alterations including infl ammatory cell infi ltration around portal triad, congestion, loss of glycogen in the hepatocytes. Additionally, degenerative cellular alterations, such as numerous vacuolizations including myelinic fi gure formation, pyknotic nuclei with peripheral localization of heterochromatin condensation and mitochondrial elongation were observed in cytoplasm of hepatocytes. CAPE signifi cantly reduced these histopathological changes. Our results indicate that CAPE should be considered in the prevention of oxidative stress in diabetic liver (Tab. 3, Fig. 4, Ref. 47). Text in PDF www.elis.sk. KEY WORDS: caffeic acid phenethyl ester, streptozotocin, liver.

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Effects of cod liver oil on tissue antioxidant pathways in normal and streptozotocin‐diabetic rats

Cited by 77 publications

References 34 publications

Hepatoprotective effects of cod liver oil against sodium nitrite toxicity in rats

Hepatoprotective effects of cod liver oil against sodium nitrite toxicity in rats

N-3 Fatty acids modulate antioxidant status in diabetic rats and their macrosomic offspring

The effects of caffeic acid phenethyl ester on streptozotocin-induced diabetic liver injury

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