Acrylamide-induced Oxidative Stress Research Articles

Protective property of mulberry digest against oxidative stress – A potential approach to ameliorate dietary acrylamide-induced cytotoxicity

The aim of this study was investigating the protective effect of mulberry digest (MBD) on acrylamide-induced oxidative stress. Composition analysis of MBD revealed that it contained six major phenolic compounds (quercetin-3-O-rutinoside, quercetin hexoside, quercetin rhamnosylhexoside hexoside, kaempferol rhamnosylhexoside, cyanidin-3-O-glucoside and cyanidin-3-O-rutinoside). After in vitro digestion, the contents of two anthocyanins were both decreased significantly, while the contents of four flavonoid glycosides were all increased. In addition, MBD was found to successfully suppress acrylamide-induced ROS overproduction, restore the mitochondrial membrane potential, and inhibit the mitochondrial membrane lipid peroxidation and glutathione depletion. More interestingly, the protective effect of MBD against acrylamide-induced oxidative damage was enhanced compared with mulberry fruits without digestion (MBE). Further study revealed that MBD enhanced the cell resistance capacity to acrylamide-induced oxidative stress, rather than its direct reaction with acrylamide. Overall, our results indicate that MBD provides a potent protection against acrylamide-induced oxidative stress.

Effect of epigallocatechin-3-gallate on acrylamide-induced oxidative stress and apoptosis in PC12 cells.

Acrylamide (ACR) is a chemical intermediate utilized in industry. ACR is also formed during heating of foods containing carbohydrates and amino acids. Therefore, humans are widely exposed to ACR, and ACR neurotoxicity in humans is a significant public health issue attracting wide attention. In this study, we investigated the potential neuroprotective effects of epigallocatechin-3-gallate (EGCG), the most abundant polyphenolic compound in green tea, in PC12 cells treated with ACR. ACR-treated PC12 cells pretreated with various concentrations of EGCG (2.5, 5 and 10 μM) for 24 h had increased viability and acetylcholinesterase activity and reduced apoptosis and necrosis compared to cells exposed to ACR alone. EGCG reduced the expression of bax mRNA, decreased cytochrome c release, reduced intracellular calcium levels, inactivated caspase 3 and increased mitochondrial membrane potential, suggesting that EGCG prevents ACR-induced apoptosis through a mitochondrial-mediated pathway. In addition, EGCG inhibited the formation of reactive oxygen species and lipid peroxidation while enhancing superoxide dismutase activity and glutathione levels, thereby reducing oxidative stress. Our results indicate that pretreatment of PC12 cells with EGCG attenuates ACR-induced apoptosis by reducing oxidative stress. Therefore, drinking green tea may reduce nerve injury induced by ACR.

In vitro gastrointestinal digestion promotes the protective effect of blackberry extract against acrylamide-induced oxidative stress

Acrylamide (AA)-induced toxicity has been associated with accumulation of excessive reactive oxygen species. The present study was therefore undertaken to investigate the protective effect of blackberry digests produced after (BBD) in vitro gastrointestinal (GI) digestion against AA-induced oxidative damage. The results indicated that the BBD (0.5 mg/mL) pretreatment significantly suppressed AA-induced intracellular ROS generation (56.6 ± 2.9% of AA treatment), mitochondrial membrane potential (MMP) decrease (297 ± 18% of AA treatment) and glutathione (GSH) depletion (307 ± 23% of AA treatment), thereby ameliorating cytotoxicity. Furthermore, LC/MS/MS analysis identified eight phenolic compounds with high contents in BBD, including ellagic acid, ellagic acid pentoside, ellagic acid glucuronoside, methyl-ellagic acid pentoside, methyl-ellagic acid glucuronoside, cyanidin glucoside, gallic acid and galloyl esters, as primary active compounds responsible for antioxidant action. Collectively, our study uncovered that the protective effect of blackberry was reserved after gastrointestinal digestion in combating exogenous pollutant-induced oxidative stress.

Assessment the Protective Role of Quercetin on Acrylamide-Induced Oxidative Stress in Rats

This study aimed to elucidate whether quercetin treatment could modulate acrylamide (ACR)-induced DNA damage and oxidative changes in rat brain, liver, kidneys and testes tissues. Fifty adult albino rats were divided into five groups. The first group served as normal control, second group received 50 mg/kg quercetin (QTN) and third group received 20 mg/kg ACR. Fourth and fifth groups received dose of ACR along with 25 or 50 mg/kg QTN, respectively. ACR and QTN were given by oral administrations for 30 days. The results showed that, ACR administration induced significant elevation of alanine transferase, aspartate transferase activities, urea, creatinine and Malondialdehyde levels in serum, whereas, Acetylcholine esterase and testosterone levels were reduced after ACR administration. Moreover, ACR treatment increased Glutathione-S-transferase, Myeloperoxidase, Glutathione peroxidase activity, 8-hydroxy deoxyguanosine, tumor necrosis factor-α and nitric oxide contents in all tissues. QTN significantly improved the previous parameters. It played a role in ameliorating toxic effects of ACR in rats by reducing oxidative stress. Practical Applications Acrylamide was found in various fried, deep fried and oven-baked foods that are regularly consumed like chips, crisps and bread, also biscuits, crackers and breakfast cereals. Acrylamide exposure led to increase of alanine transferase, aspartate transferase activities, urea, creatinine and Malondialdehyde levels in serum, whereas, Acetylcholine esterase and testosterone levels were reduced. Moreover, ACR treatment increased Glutathione-S-transferase, Myeloperoxidase, Glutathione peroxidase activity, 8-hydroxy deoxyguanosine, tumor necrosis factor-α and nitric oxide contents in all tissues. Our study revealed the protective role of quercetin on acrylamide-induced oxidative stress in rats. Quercetin regulate the generation of inflammatory markers and increasing antioxidant enzyme activity in rat liver, kidneys, brain and testes tissues.

The chemoprotection of a blueberry anthocyanin extract against the acrylamide-induced oxidative stress in mitochondria: unequivocal evidence in mice liver.

Acrylamide (AA) is one of the most important contaminants occurring in heated food products. Accumulating evidence indicates that AA-induced toxicity is associated with oxidative stress and long-term exposure to AA induced mitochondria collapse and finally leads to apoptosis. Whereas anthocyanins are natural antioxidants and have a strong ability to reduce oxidative damage in vivo. This study investigates the protection of a blueberry anthocyanin extract (BAE) against AA-induced mitochondrial oxidative stress in mice models. The activities of electron transport chain complexes, oxidative status, and the structure and function of mitochondria were measured. Results showed that pretreatment with BAE markedly inhibited reactive oxygen species (ROS) formation, and prevented the successive events associated with the mitochondrial damage and dysfunction, including recovered activities of electron transport chain, ATPase and superoxide dismutase, ameliorated depolarization of mitochondrial membrane potential and membrane lipid peroxidation, reduced release of cytochrome c and protection of mitochondria against swelling. In a word, mitochondria are a key target at the organelle level for the protective effect of BAE against AA toxicity. These results will be helpful to provide new clues for a better understanding of the AA toxicity intervention mechanism and for exploring effective dietary constituents for intervention of AA toxicity.

Hispidin derived from Phellinus linteus affords protection against acrylamide-induced oxidative stress in Caco-2 cells

Acrylamide (AA), a well-known toxicant, has attracted numerous attentions for its presumably carcinogenesis, neurotoxicity and cytotoxicity. Oxidative stress was considered to be associated with acrylamide cytotoxicity, but the link between oxidative stress and acrylamide cytotoxicity is still unclear. In the present study, hispidin produced from the edible fungus Phellinus linteus displayed dramatically antioxidant activities against DPPH radicals, ABTS radicals, ferric reducing and hydroxyl radicals, as well as superoxide anion radicals. Moreover, the cytoprotective effect of hispidin against AA-induced oxidative stress was verified upon Caco-2 cells according to evaluate the cell viability, intracellular ROS, mitochondrial membrane potential (MMP) and glutathione (GSH) in the presence or absence of AA (5mM) in a dose-dependent manner. Collectively, our results demonstrated for the first time that hispidin was able to inhibit AA-induced oxidative stress, which might have implication for the dietary preventive application.

Antioxidant and immunostimulant effect of carica papaya linn. Aqueous extract in acrylamide intoxicated rats.

Introduction:The present study was conducted to evaluate the antioxidant and immunostimulant effects of The Carica papaya fruit aqueous extract (CPF, Caricaceae) against acrylamide induced oxidative stress and improvement of Immune functions which affected by free radicals liberating acrylamide in rats.Material and methods:Sixty male wistar albino rats (195-230g) were assigned to four groups, (fifteen/group). The first group used as control group and received normal physiological saline orally daily. The second group was supplemented with acrylamide 0.05% in drinking water. The third group was gastro-gavaged with 250 mg/kg of papaya fruit extract orally on daily basis. The fourth group was supplemented with acrylamide 0.05% in drinking water and gastro-gavaged with 250 mg/kg of papaya fruit extract orally on daily basis. The chosen dose of papaya fruit extract was based on the active pharmacological dose range obtained from the orientation study earlier conducted. The experimental period was extended to forty day. At the expiration of the experimental period and night fasting, blood samples were collected from the orbital venous sinus. The sera were separated and used for determining of IgG and IgM and the stomach, liver and kidney homogenates for estimation of MDA, GSH level, SOD and CAT activity as a biomarker of lipid peroxidation and antioxidative stress.Results and discussion:The obtained results revealed that, acrylamide caused significant increases in MDA and decrease of GSH level, SOD and CAT activity due to the oxidative stress induced by acrylamide on membrane polyunsaturated fatty acids in rat’s stomach, liver and kidney while administration of CPF aqueous extract, was significantly ameliorated the increased levels of MDA and decline of GSH, SOD and CAT activity in the stomach, liver and kidney tissues caused by acrylamide toxicity. Meanwhile, CPF aqueous extract significantly increased immune functions (IgG and IgM) while acrylamide significantly decrease it specially IgG. Thus, this study suggests that acrylamide-induced oxidative stress in rats can be ameliorated by administration of CPF aqueous extract.

Protective effect of N-acetyl-L-cysteine against acrylamide-induced oxidative stress in rats

Acrylamide (AA), used in many fields, from industrial manufacturing to laboratory work, is also formed during the heating process through the interactions of amino acids. Therefore, AA poses a significant risk for both human and animal health. This study aimed to elucidate whether N-acetyl-L-cysteine (NAC) treatment could modulate AA-induced oxidative changes in the brain, lung, liver, kidney, and testes tissues of the rat. Rats were divided into 4 groups, as the control (C), NAC [150 mg/kg intraperitoneally (i.p.)], AA (40 mg/kg i.p.), and NAC + AA groups. After 10 days, the rats were decapitated and the tissues were excised. Malondialdehyde (MDA) and glutathione (GSH) levels, and myeloperoxidase activity (MPO) were determined in the tissues, while oxidant-induced tissue fibrosis was determined using the collagen contents. Serum enzyme activities, cytokine levels, and leukocyte apoptosis were assayed in the plasma. In the AA group, GSH levels decreased significantly, while the MDA levels, MPO activity, and collagen content increased in the tissues suggesting oxidative organ damage. In the NAC + AA group, oxidant responses reversed significantly. Serum enzyme activities, cytokine levels, and leukocyte apoptosis, which increased following AA administration, decreased with NAC treatment. Therefore, supplementing with NAC can be useful when there is a risk of AA toxicity, as NAC inhibits neutrophil infiltration, balances the oxidant-antioxidant status, and regulates the generation of inflammatory mediators to protect tissues.

Resveratrol ameliorates oxidative DNA damage and protects against acrylamide-induced oxidative stress in rats

Acrylamide (ACR), used in many fields from industrial manufacturing to laboratory personnel work is also formed during the heating process through interactions of amino acids. Therefore ACR poses a significant risk to human health. This study aimed to elucidate whether resveratrol (RVT) treatment could modulate ACR-induced oxidative DNA damage and oxidative changes in rat brain, lung, liver, kidney and testes tissues. Rats were divided into four groups as control (C); RVT (30mg/kg i.p. dissolved in 0.9% NaCl), ACR (40mg/kg i.p.) and RVT+ACR groups. After 10days rats were decapitated and tissues were excised. 8-hydroxydeoxyguanosine (8-OHdG) is a biomarker of oxidative DNA damage. 8-OHdG content in the extracted DNA solution was determined by enzyme-linked immunosorbent assay method. Malondialdehyde (MDA), glutathione (GSH) levels and myeloperoxidase activity (MPO) were determined in tissues, while oxidant-induced tissue fibrosis was determined by collagen contents. Serum enzyme activities, cytokine levels, leukocyte apoptosis were assayed in plasma. As an indicator of oxidative DNA damage, 8-OHdG levels significantly increased in ACR group and this was reversed significantly by RVT treatment. In ACR group, GSH levels decreased significantly while the MDA levels, MPO activity and collagen content increased in the tissues suggesting oxidative organ damage. In RVT-treated ACR group, oxidant responses reversed significantly. Serum enzyme activities, cytokine levels and leukocyte late apoptosis which increased following ACR administration, decreased with RVT treatment. Therefore supplementing with RVT can be useful in individuals at risk of ACR toxicity.

Enhanced role of elaidic acid on acrylamide-induced oxidative stress in epididymis and epididymal sperm that contributed to the impairment of spermatogenesis in mice

Acrylamide (ACR) and trans fatty acids (TFA) could be found co-existent in many foods processed by high temperature. Our study investigated effect of elaidic acid (ELA), the predominant TFA, on deficits of spermatogenesis induced by ACR. Results showed that ELA enhanced the decreases of spermatogonia along with mature sperms after treatment of ACR, and that spermatozoa quality was significantly reduced by addition of ELA to mice treated with ACR. Moreover, ELA play an enhancing role in ACR-induced up-regulating of malondialdehyde (MDA) level in epididymal sperm and cauda epididymides, also up-regulating of protein carbonyls (PCOs) level in cauda epididymides. Meanwhile, ELA play an enhancing role in ACR-induced reducing of activity of superoxide dismutases (SOD) in epididymal sperm, corpus and cauda epididymides, also the reducing of activity of glutathione peroxidase (GPx) in cauda epididymides. These data suggest that ELA enhances ACR-induced oxidative stress in the epididymis and epididymal sperm of mice and has subsequent effect on spermatogenesis in mice testis.

Enhanced fat consumption potentiates acrylamide-induced oxidative stress in epididymis and epididymal sperm and effect spermatogenesis in mice

Acrylamide (ACR) and high contents of fat could be found co-existent in many foods processed by high temperature, such as deep-frying and roasting. This study investigated the effect of enhanced fat consumption on deficits of spermatogenesis induced by ACR, and explored potential mechanisms of oxidative damage involved in this pathology in mice. Results show that enhanced feeding of corn oil and pork fat on mice potentiated the decreases of spermatogonia along with mature sperms after treatment of ACR, and that spermatozoa quality is significantly reduced as a result of enhanced feeding of corn oil and pork fat on mice treated with ACR. Moreover, enhanced consumption of corn oil and pork fat potentiated the up-regulation of malondialdehyde (MDA) level in epididymal sperm and cauda epididymides, also up-regulated level of Protein carbonyls (PCOs) in cauda epididymides, of mice after treatment of ACR. Last, enhanced consumption of corn oil and pork fat potentiated the reduced activity of superoxide dismutases (SOD) in epididymal sperm, corpus, and cauda epididymides, also reduced activity of glutathione peroxidase (GPx) in cauda epididymides, of mice treated with ACR. These data suggest that enhanced feeding of corn oil and pork fat on mice potentiates ACR-induced oxidative stress in the epididymis and epididymal sperm and a subsequent effect on spermatogenesis.

Acrylamide-induced oxidative stress in human erythrocytes

Acrylamide (AA), a widely used industrial chemical, is shown to be neurotoxic, mutagenic and carcinogenic. This study was carried out to investigate the effects of different doses of AA on lipid peroxidation (LPO), haemolysis, methaemoglobin (MetHb) and antioxidant system in human erythrocytes in vitro. Erythrocyte solutions were incubated with 0.10, 0.25, 0.50 and 1.00 mM of AA at 37 degrees C for 1 hour. At the end of the incubation, malondialdehyde (MDA), an end product of LPO, was determined by liquid chromatography (LC) while total glutathione, reduced glutathione (GSH) levels, activities of superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GSH-Px) enzymes and the rates of haemolysis and MetHb were determined by spectrophotometric methods. All of the studied concentrations of AA increased MetHb formation and SOD activity, and induced MDA formation and haemolysis due to the destruction of erythrocyte cell membrane. AA caused a decrease in the activities of GSH-Px, CAT and GSH levels. However, these effects of AA were seen only at higher concentrations than AA intake estimated for populations in many countries. We suggest that LPO process may not be involved in the toxic effects of AA in low concentrations, although the present results showed that the studied concentrations of AA exert deteriorating effects on antioxidant enzyme activities, LPO process and haemolysis.

The moderating role of dark soy sauce to acrylamide-induced oxidative stress and neurophysiological perturbations in rats

To evaluate the protective effects of dark soy sauce (DSS) against acrylamide (ACR)-induced neurotoxicity in rats, 60 adult Sprague Dawley female rats were given DSS (0.5 ml/kg body weight/day) before, after, and during ACR treatment (10 mg/kg body weight/day) for 8 weeks in total. Treatment only with ACR resulted in a significant increase in lipid peroxidation level, lactate dehydrogenase, and serum creatine kinase activity, but a significant decrease in superoxide dismutase activity in brain homogenate. Moreover, serum serotonin, corticosterone, 3, 5, 3′-triiodothyronine, and L-thyroxine, thyroid stimulating hormone, estradiol, progesterone, and plasma adrenaline decreased significantly in ACR rats. Treatment with DSS before, during, and after ACR treatment partially antagonized the effects induced by ACR. In conclusion, DSS exhibited a protective action against ACR-induced oxidative stress and biochemical perturbations in rats; and treatment with DSS during ACR exposure was more effective than after or before ACR treatment.

Acrylamide-induced oxidative stress and biochemical perturbations in rats

Acrylamide is neurotoxic to experimental animals and humans. Also, it has mutagenic and carcinogenic effects. The present study was carried out to investigate the effects of different doses of acrylamide on some enzyme activities and lipid peroxidation in male rats. Animals were assigned at random to one of the following treatments: group 1 served as control, while groups 2, 3, 4, 5, 6 and 7 were treated with 0.5, 5, 25, 50, 250 and 500 μg/kg body weight of acrylamide, respectively in drinking water for 10 weeks. Acrylamide significantly decreased plasma protein levels and the activity of creatine kinase, while increased plasma phosphatases. The activities of transaminases and phosphatases were significantly decreased in liver and testes, while lactate dehydrogenase did not change compared to control group. Plasma and brain acetylcholinesterase activity was significantly decreased. The concentration of thiobarbituric acid reactive substances, and the activities of glutathione S-transferase and superoxide dismutase in plasma, liver, testes, brain, and kidney were increased in acrylamide-treated rats. On the other hand, results obtained showed that acrylamide significantly reduced the content of sulfhydryl groups and protein in different tissues. The present results showed that different doses of acrylamide exerted deterioration effects on enzyme activities and lipid peroxidation in a dose-dependent manner.