Assessment of Alterations in Antioxidant Enzymes and Histology of Liver and Cerebral Cortex of Developing Chick Embryo in Acrylamide Toxicity (original) (raw)
Related papers
Effect of acrylamide on chick embryonic liver glutathione S-transferases
Mediterranean Journal of Nutrition and Metabolism, 2010
Glutathione S-transferases (GSTs, EC 2.5.1.18), as the detoxifying enzymes, play an important protective role in embryonic tissues. The GSTs of eleventh-day chick embryonic liver were purified to electrophoretic homogeneity with an overall yield of 31%. The SDS-PAGE analysis of chick embryonic liver GSTs resolved in to three bands, CL1, CL2 and CL3, with relative molecular weights of 27.0, 26.0 and 25.0 kDa respectively. On 72 hours of treatment with acrylamide (AC) (0.1, 0.2 and 0.3 mg) the specific activities of GSTs with CDNB, pNBC, EPNP, BSP, Δ55A and pNPA increased significantly. Total GPx levels were decreased with CHP in liver samples. Immunoblot analysis of AC-treated liver samples showed a dose-dependent increase in the induction of GSTs. CL1 of theta class, CL2 of Mu class and CL3 of alpha class were induced with AC treatment. The theta, mu and alpha classes induced by AC might inhibit the initiation of carcinogenesis.
Alteration of Oxidative Status in Rats Following Administration of Acrylamide
2007
Introduction: Acrylamide (ACR) is a known industrial neurotoxic and carcinogenic chemical in rodents. The recent discovery of acrylamide in wide variety of commonly consumed foods has energized research efforts worldwide to define toxic mechanisms. Objective: The present study is carried out to investigate the effect of acrylamide administration on in vivo malondialdehyde (MDA, a product of lipid peroxidation), reduced glutathione (GSH) as well as copper and zinc superoxide dismutase enzyme activity (Cu/Zn SOD) of rats. Material and Methods: Fourteen adult male Sprague Dawley rats were divided into two groups each containing "7" rats. Group 1 served as negative control fed on basal diet and group 2 (positive control) received basal diet and acrylamide (0.34g/ kg diet) for 11 days. Levels of MDA, GSH and activity of SOD were determined in liver, kidneys, brain, heart, testes, spleen and lungs of rats. Results: ACR treatment significantly increased MDA in all organs; the hig...
Scientific Reports
Acrylamide (ACR) is a toxic compound commonly found in fried, baked and heat-processed starchy foods. The current study investigated the time-dependent effects of maternal exposure to non-toxic ACR doses on the oxidative stress, liver function, and basal blood morphology of the rat offspring. Pregnant, Wistar rats were randomly divided into the control group or the groups administrated with ACR (3 mg/kg b.w./day): long exposure for 15 days, medium exposure for 10 days and short exposure for 5 days during pregnancy. Body mass, blood morphology and hematology, serum concentrations of growth hormone, IGF-1, TNF-α, IL-1β, IL-6 and insulin, liver histomorphometry, liver activity of beclin1, LC2B and caspase3, markers of oxidative stress and the activity of antioxidative enzymes in blood serum and the liver were measured in offspring at weaning (postnatal day 21). Even short prenatal exposure to ACR led to oxidative stress and resulted in changes in liver histomorphometry and upregulation...
Mechanisms for the Induction of Oxidative Stress in Syrian Hamster Embryo Cells by Acrylonitrile
Toxicological Sciences, 2002
Chronic administration of acrylonitrile to rats resulted in an increase in the incidence of glial neoplasms of the brain. Recent studies have shown that acrylonitrile induces oxidative stress in rat brain and cultured rat glial cells. Acrylonitrile also induces morphological transformation concomitant with an increase in the formation of oxidized DNA in Syrian Hamster Embryo (SHE) cells in a dose-dependent manner. The mechanism for the induction of oxidative stress in SHE cells remains unresolved. The present study examined the effects of acrylonitrile on enzymatic and nonenzymatic antioxidants in SHE cells. SHE cells were treated with subcytolethal doses of acrylonitrile (0, 25, 50, and 75 g/ml) for 4, 24, and 48 h. Acrylonitrile (50 g/ml and 75g/ml) increased the amount of reactive oxygen species in SHE cells at all time points. Glutathione (GSH) was depleted and catalase and superoxide dismutase activities were significantly decreased in SHE cells after 4 h of treatment. The inhibition of these antioxidants was temporal, returning to control values or higher after 24 and 48 h. Xanthine oxidase activity was increased following 24 and 48 h treatment with acrylonitrile. 1-aminobenzotriazole, a suicidal P450 enzyme inhibitor, attenuated the effects of acrylonitrile on catalase and xanthine oxidase in SHE cells, suggesting that P450 metabolism is required for acrylonitrile to produce its effects on these enzymes. Additional studies showed that in the absence of metabolic sources acrylonitrile had no effect on either catalase or superoxide dismutase activity. These results suggest that the induction of oxidative stress by acrylonitrile involves a temporal decrease in antioxidants and increase in xanthine oxidase activity that is mediated by oxidative metabolism of acrylonitrile.
Acrylamide-induced oxidative stress and biochemical perturbations in rats
Toxicology, 2006
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 g/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.
Toxicology and Applied Pharmacology, 1982
Effect of acrylamide on rat hepatic and brain mixed-function oxidases and ghttathione-9transferase was investigated. Administration of acrylamide (25 mg/kg) for 7,14,2 1, and 28 days showed no significant effect on hepatic and brain mixed-function oxidases at 7 days whereas a slight increase in the activity of hepatic glutathione-9transferase was observed. Brain ghttathione-S-transferase remained unaffected at this treatment schedule. At 14 days of acrylamide exposure, all the hepatic mixed-function oxidases with the exception of aminopyrine-Ndemethylase and brain aryl hydrocarbon hydroxylase showed a decrease, and by 2 1 days all the hepatic and brain mixed-function oxidases were significantly decreased. The decrease in enzyme activities was also evident at 28 days of acrylamide treatment. Hepatic glutathione-Stransferase returned to normal level at 14 days of acrylamide exposure. Both hepatic and brain GST showed a significant decrease at 2 1 and 28 days of acrylamide treatment. Administration of acrylamide at 50 mg/kg for 3,6, and 10 days produced no changes in hepatic and brain ghuathioneStransferase activity at early time periods (3 and 6 days). A significant decrease in glutathione-S-transferase activity of both tissues was seen at 10 days of acrylamide exposure. Hepatic mixed-function oxidases showed no change at 3 days but significant decrease at 6 and 10 days of acrylamide exposure. Brain mixed-function monooxygenase activity at this dose was inhibited even after 3 days of acrylamide treatment. The results suggest that acrylamide interferes with xenobiotic metabolism in both liver and brain.
A histological study on acrylamide and cadmium chloride altered chick embryonic liver
IOSR Journal of Pharmacy (IOSRPHR), 2012
Histology is the study of the microscopic anatomy of cells and tissues. The present study was made on control and treated chick embryonic liver tissues using toxic compounds like acrylamide (AC) & cadmium chloride (Cd), on the morphological modification of embryonic liver and hepatic cells. The metal ion, Cd, had severe damaging effect on chick embryonic liver than AC and however our study has revealed that these two are causing damage to the embryos.
PloS one, 2017
High acrylamide (ACR) content in heat-processed carbohydrate-rich foods, as well as roasted products such as coffee, almonds etc., has been found to be as a risk factor for carcinogenicity and genotoxicity by The World Health Organization. Glycidamide (GLY), the epoxide metabolite of ACR, is processed by the cytochrome P-450 enzyme system and has also been found to be a genotoxic agent. The aim of this study was to determine whether ACR and/or GLY have any detrimental effect on the meiotic cell division of oocytes. For this purpose, germinal vesicle-stage mouse oocytes were treated with 0, 100, 500, or 1000 μM ACR or 0, 25, or 250 μM GLY in vitro. In vivo experiments were performed after an intraperitoneal injection of 25 mg/kg/day ACR of female BALB/c mice for 7 days. The majority of in vitro ACR-treated oocytes reached the metaphase-II stage following 18 hours of incubation, which was not significantly different from the control group. Maturation of the oocytes derived from in viv...
Acrylamide toxicity in isolated rat hepatocytes
Toxicology in Vitro, 1998
AbstractÐAcrylamide (ACR) is an important industrial chemical used primarily in the production of polymers and co-polymers. Acrylamide is mainly neurotoxic to experimental animals as well as humans and has also been shown to be mutagenic and carcinogenic. The present study was designed to investigate the toxicity of ACR on isolated rat hepatocytes. The hepatocytes were isolated by collagenase perfusion method and were incubated with dierent concentrations of ACR (0.1, 1, 10 mM) for 2 hours. Cell viability by trypan blue exclusion and leakage of the enzymes such as alanine transaminase (ALT) and aspartate transaminase (AST) were determined. Reduced glutathione (GSH), glutathione S-transferase (GST) activity were also measured. A signi®cant decrease in the cell viability was observed after exposure to 10 mM ACR for 30 min, while 1 mM ACR caused a signi®cant decrease in the viability after 60 min. ALT leakage was parallel to the cell viability. AST leakage was signi®cantly increased at 30 min of incubation with 10 mM ACR, whereas 2 hours of incubation was required for the leakage of AST from rats hepatocytes with 1 mM ACR. 10 mM ACR decreased signi®cantly GSH as early as 30 min, while GSH level was decreased at 60 min after exposure to 1 mM ACR. Also, the GST activity increased with increasing the dose of ACR. Cytochrome P450 concentration was decreased after exposure to 10 mM ACR. The eect of ACR on cell viability, ALT and AST leakage, GSH and GST activity was time and dose dependent. # Abbreviations: ACR = acrylamide; ALT = alamine transaminase; AST = aspartate transaminase; BSA = bovine serum albumin; GSH = glutathione; GST = glutathione S-transferase.