Antioxidant effect of vitamin E and 5-aminosalicylic acid on acrylamide induced kidney injury in rats

Rajeh, Nisreen; Al-Dhaheri, Najlaa M.

doi:10.15537/smj.2017.2.16049

Cited by 36 publications

(19 citation statements)

References 14 publications

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“…In contrast to its toxic effect on dopaminergic neurons, LC 50 of ACR had no effect on LDH release into the culture medium and only caused significant LDH release at the concentration of 2 mM compared to untreated control cultures. These results agree with some other studies reporting no significant effect of ACR on LDH activity [22,29]. um indicates, to some extent, the selective effect on dopaminergic neurons and absence of overall toxicity on primary mesencephalic cell culture.…”

Section: Discussionsupporting

confidence: 93%

Neurotoxic effects of acrylamide on dopaminergic neurons in primary mesencephalic cell culture

Radad

Al‐Shraim

Al-Emam

et al. 2019

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Introduction: Exposure to acrylamide is increasing worldwide as a result of its heavy use in industry and formation in carbohydrate-rich food cooked at high temperature. Despite its neurotoxicity, no studies have shown its toxic effects on dopaminergic neurons yet. Therefore, the current study was carried out to show whether acrylamide adversely affects primary cultured dopaminergic neurons. Material and methods: Acrylamide (0.001, 0.01, 0.1, 1, 2 mM) was added to two different groups of primary mesencephalic cell cultures on the 9 th day in vitro for 24 and 48 h, respectively. Moreover, a group of cultures was treated with lower concentrations of acrylamide (0.01, 0.05, 0.1, 0.5 mM) on the 6 th day in vitro for 5 consecutive days to investigate its long-term effects on dopaminergic neurons. Following each treatment, culture media were obtained for measuring lactate dehydrogenase, and cultured cells were stained immunocytochemically against tyrosine hydroxylase and neuronal nuclear antigens. Results: Treatment of cultures with acrylamide for 48 h significantly reduced the number of dopaminergic neurons, adversely altered the morphology of the surviving neurons and increased levels of lactate dehydrogenase in the culture media. Similar treatment of cultures with acrylamide also resulted in lower numbers of total neuronal cells as shown by a reduced expression of the neuronal nuclear antigen. Prolonged treatment of cultures with lower concentrations of acrylamide slightly reduced the survival of dopaminergic neurons but increased the release of lactate dehydrogenase into the culture media as well. Conclusions: The current study shows, for the first time, neurotoxicity of acrylamide on dopaminergic neurons in the primary mesencephalic cell culture.

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Section: Discussionsupporting

confidence: 93%

Neurotoxic effects of acrylamide on dopaminergic neurons in primary mesencephalic cell culture

Radad

Al‐Shraim

Al-Emam

et al. 2019

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“…Acrylamide. The dose of ACR used was 45 mg/kg/ /day [31]. Acrylamide (99% pure) was purchased from Sigma Chemical Company (St. Louis, Missouri, USA).…”

Section: Chemicalsmentioning

confidence: 99%

Acrylamide-induced adverse cerebellar changes in rats: possible oligodendrogenic effect of omega 3 and green tea

Imam

Gadallah

2019

Folia Morphol

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Background: Humans are widely exposed to acrylamide (ACR) and its neurotoxicity is a significant public health issue attracting wide attention. The aim of the study was to investigate ACR-induced adverse cerebellar changes in rats and study the possible oligodendrogenic effect of omega 3 and green tea. Materials and methods: Twenty-four adult albino rats weighing 150-200 g were randomly divided into four equal groups (6 rats each): control group (Group I), the rats that received ACR 45 mg/kg/day (Group II), the rats that received ACR concomitant with omega 3 at a dosage of 200 mg/kg/day (Group III), the rats that received ACR concomitant with green tea dissolved in drinking water at a dosage of 5 g/L (Group IV). The rats were euthanized after 8 weeks of the experiment. Malondialdehyde (MDA) and glutathione (GSH) were measured in cerebellar homogenates. Sections of 5 µm thickness from specimens from the cerebellum were stained with haematoxylin and eosin, silver stain and immunohistochemical stains: platelet-derived growth factor alpha (PDGFα; for oligodendrocytes), glial fibrillary acidic protein (GFAP; for astrocytes) and BCL2 (antiapoptotic). Results: Omega 3 and green tea had improved MDA and GSH as compared to the ACR group. Histologically, the ACR group showed variable degrees of cellular degeneration. Omega 3 had induced oligodendrogenesis in Group III. The optical density of silver stain was significantly (p < 0.05) increased in Groups III and IV as compared to the ACR group. Area per cent of positive PDGFα was significantly increased in the ACR + omega 3 group as compared to the ACR group. Area per cent of positive GFAP was significantly decreased in Groups III and IV as compared to the ACR group. Area per cent of positive BCL2 was significantly increased in the omega 3-trated group as compared to the ACR group. Conclusions: Concomitant administration of omega 3 or green tea with ACR might mitigate the adverse cerebellar changes caused by ACR thanks to an oligodendrogenic effect of omega 3. (Folia Morphol 2019; 78, 3: 564-574)

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“…[ 43 ] Vit E is the key antioxidant component of spermatozoa and membrane protectants against ROS[ 43 44 ] and could be considered as a good prophylactic agent against AA-induced toxicity. [ 45 46 ]…”

Section: Discussionmentioning

confidence: 99%

Histological and ultrastructure study of the testes of acrylamide exposed adult male albino rat and evaluation of the possible protective effect of Vitamin E intake

Hasanin

Sayed

Ghoneim

et al. 2018

J Microsc Ultrastruct

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Acrylamide (AA) is a hazardous unavoidable gonadal toxin. Hence, the aim of this study is to clarify its harmful effects on the testis of adult albino rat by light and electron microscope and to evaluate the possible role of Vitamin E (Vit E) in the prevention of such effects. Thirty-five adult male albino rats were enrolled in this study. They were divided into three groups: Group I (control); Group II (AA exposed), and Group III (AA and concomitant Vit E treated group). Animals of Groups II and III were further subdivided into two equal subgroups (each subgroup included five rats): (a) rats were sacrificed after 4 weeks and (b) rats were sacrificed after 6 weeks. The testes of each rat were dissected out, processed, and examined by Hematoxylin and Eosin, Periodic acid–Schiff and Mallory's trichrome stains as well as electron microscopic study. The study revealed that AA induces testicular damage at the histological and ultrastructural level in the form of degeneration and arrested spermatogenesis. Moreover, decreased seminiferous tubules diameters and epithelial height were detected. These changes are maximally improved in Vit E treated group. Hence, we could conclude that AA causes degenerative changes of the testes of albino rats and arrest of spermatogenesis. The AA-induced histological and ultrastructural changes of the testes could be explained by oxidative stress. These effects changes are proportional to the duration of exposure. Moreover, it could be concluded that Vitamin E has a protective role against AA-induced testicular damage by its antioxidant and anti-apoptotic effects.

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Antioxidant effect of vitamin E and 5-aminosalicylic acid on acrylamide induced kidney injury in rats

Cited by 36 publications

References 14 publications

Neurotoxic effects of acrylamide on dopaminergic neurons in primary mesencephalic cell culture

Neurotoxic effects of acrylamide on dopaminergic neurons in primary mesencephalic cell culture

Acrylamide-induced adverse cerebellar changes in rats: possible oligodendrogenic effect of omega 3 and green tea

Histological and ultrastructure study of the testes of acrylamide exposed adult male albino rat and evaluation of the possible protective effect of Vitamin E intake

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