Toxic Effects Of Acrylamide Research Articles

The Biological, Biochemical, and Immunological Impact of Broccoli and Green Pea Sprouts on Acrylamide Intoxicated Rats

Consuming plant sprouts as part of the daily human diet is slowly on the increase, and the health benefits are now of interest in several disciplines. The aim of this investigation was to evaluate the chemical compositions of dried broccoli or dried green pea sprouts and the subsequent effects on the biological, biochemical and immunological parameters of male albino rats supplemented with acrylamide as a toxic material. Chemical constituents, mineral contents, total phenols and total flavonoid of tested vegetable sprouts were analyzed. Thirty male albino rats weighting 160± 5 g. were separated into 6 groups. The negative control group was first, and then the second group was given acrylamide 2.5 μg/kg/day. Groups (3, 4) and (5,6) were given treatment of the same toxic material and received 5 and 10 g dried broccoli and pea sprouts per 100 g basal diet, respectively. Feed intake, body weight gain, FER and some organs weights were calculated towards the conclusion of the investigation. Also, liver enzymes, lipids profile, serum glucose, kidney function, brain enzymes, oxidative activity and immunoglobulin were determined. Results showed that tested sprouts had high protein, fiber, vital minerals, total phenols and total flavonoid components. In addition, there were significant positive effects on the biochemical parameters that were tested, such as lipids profile, serum glucose, liver function, kidney functions, oxidative activity, brain enzyme and immunity responses, particularly at the 10% level, of tested sprouts and pea sprouts had high effect on tested parameters more than broccoli sprouts. In conclusion, pea and broccoli sprouts could potentially be used as protective agents against the toxic effect of acrylamide and the obtained results suggested that tested sprouts can be used as ideal candidates of natural antioxidant agents.

Toxic Effects of Acrylamide on Human Health: A Review Article

Toxic Effects of Acrylamide on Human Health: A Review Article

ОЦЕНКА ВЛИЯНИЯ АКРИЛАМИДА НА ЭКСПРЕССИЮ ГЕНА HMOX В ПЕЧЕНИ КРЫС

Acrylamide is a synthetic material that is widely used in industry. It is formed during the heating process. Acrylamide is a geno- and cytotoxic compound, which is a carcinogen. So far, in vivo studies have focused on the toxic effects of acrylamide at high doses. In the present study, the toxic effects caused by acrylamide were studied at those doses when clinical signs did not yet appear.

Effect of Acrylamide Supplementation on the Population of Vasoactive Intestinal Peptide (VIP)-Like Immunoreactive Neurons in the Porcine Small Intestine.

Acrylamide is one of the harmful substances present in food. The present study aimed to establish the effect of acrylamide supplementation in tolerable daily intake (TDI) dose (0.5 µg/kg b.w./day) and a dose ten times higher than TDI (5 µg/kg b.w./day) on the population of vasoactive intestinal peptide-like immunoreactive (VIP-LI) neurons in the porcine small intestine and the degree of the co-localization of VIP with other neuroactive substances (neuronal nitric oxide synthase (nNOS), substance P (SP), and cocaine- and amphetamine-regulated transcript peptide (CART)). In our work, 15 Danish landrace gilts (5 in each experimental group) received capsules (empty or with low or high doses of acrylamide) for a period of 28 days with their morning feeding. Using double immunofluorescence staining, we established that acrylamide supplementation increased the number of neurons showing immunoreactivity towards VIP in all types of enteric nervous system (ENS) plexuses and fragments of the small intestine studied. Moreover, both doses of acrylamide led to changes in the degree of co-localization of VIP with nNOS, SP, and CART in intramural neurons. The observed changes may be the adaptation of neurons to local inflammation, oxidative stress, or the direct toxic effects of acrylamide on intestinal neurons, also referred to as neuronal plasticity.

Vitamin C inhibits glycidamide-induced genotoxicity and apoptosis in Sertoli cells.

Exposure to the food contaminant acrylamide and its reactive epoxide metabolite glycidamide (GA) induces reactive oxygen species (ROS)-mediated oxidative stress and subsequent cellular death. Recent studies have revealed that the toxic effects of acrylamide may be due to GA, especially on male reproductive system cells. In this regard, it is important to determine the effects of GA on Sertoli cells, which are essential cells for the male reproductive system. Antioxidants should be consumed in sufficient quantities to minimise the effects of environmental pollutants. This study aimed to determine the direct toxic effects of GA and protective effects of vitamin C (VitC) against GA-induced damage in Sertoli cells by measuring cell viability, cytotoxicity, lipid peroxidation, ROS, antioxidant enzyme levels, apoptosis and DNA damage. Sertoli cells were exposed to GA for 24 hours at four different concentrations (ranging between 1 and 1000 μM) and in addition to these GA concentrations to VitC (50 μM). The results of cytotoxicity markers, such as cell viability and lactate dehydrogenase (LDH) showed that GA significantly reduced cell viability and increased LDH levels. We also found that GA induced overproduction of intracellular ROS, increased lipid peroxidation in cellular membrane and triggered cell apoptosis and genotoxicity. In addition, VitC supplementation ameliorated the adverse effects of GA on Sertoli cells. Consequently, these findings suggest that GA may damage the cell function in Sertoli cells, depending on the concentration. Additionally, it was evidenced that VitC has an ameliorative effect on toxicity caused by GA.

Histological Study of Toxic Effects of Acrylamide on the Liver and Kidney of Adult Male Albino Rats

Histological Study of Toxic Effects of Acrylamide on the Liver and Kidney of Adult Male Albino Rats

Cinnamon extract supplementation improves inflammation and oxidative stress induced by acrylamide: An experimental animal study.

Toxic effects of acrylamide on body organs incline researches to prevent or decrease these effects. The objective of the present study was to evaluate the effects of cinnamon extract (CE) supplementation on inflammation and oxidative stress induced by acrylamide in rats. Thirty two rats were divided into four groups as follow 1) The control group received distilled water, 2) Acrylamide- intoxicated group was administrated with 35 ml/kg/day acrylamide for two weeks, 3) Acrylamide- intoxicated rats treated with CE 250 mg/kg/day for 28 days, and 4) Acrylamide- intoxicated rats treated with CE 500 mg/kg day for 28 days. Fasting blood sample was obtained for subsequent analysis. The results showed that acrylamide- intoxicated group had significantly higher levels of malondialdehyde, tumor necrosis factor alpha, high sensitive C reactive protein, leptin and alanine transaminase (p<0.05 to p<0.01) and lower levels of total antioxidant capacity compared to the control group; whereas, cinnamon extract administration remedied levels of total antioxidant capacity, malondialdehyde, tumor necrosis factor alpha, high sensitive C reactive protein and leptin in the treatment groups, but it did not have a significant effect on adiponectin and liver enzymes (p>0.05). This study suggests that cinnamon extract may potentially be effective as a dietary source of bioactive compounds for managing acrylamide intoxication.

Effect of Acrylamide on the Tongue Musculature of Adult Male Albino Rat and the Possible Protective Role of Vitamin E: Light and Electron Microscopic Study

Abstract Background: Acrylamide is a potent toxin and carcinogen, its hazards result from its increased accumulation in the process of cooking food materials. Aim of Study: This study aimed to demonstrate the effects of acrylamide on the skeletal muscle fibers of adult male albino rat tongue for two different durations, using light and electron microscopic study and to investigate the possible protective effect of Vitamin E co-administration. Material and Methods: Sixty adult male albino rats were divided into six groups, each group included ten rats. Group I (control). Group II (Sham control). Group III received acrylamide for 20 days. Group VI received acrylamide for 40 days. Group V received acrylamide and Vitamin E, with 30 minutes interval between the two doses, for 20 days. Group VI received acrylamide and Vitamin E with 30 minutes interval between the two doses, for 40 days. All medications were given orally by gastric gavage. At the end of the experiment the tongue was dissected out for light and electron microscopic studies. Results: Light microscopic examination revealed that acrylamide lead to skeletal muscle damage in rat tongue. In the form of, fragmentations, splitting and inflammatory cellular infiltrations. Electron microscopic study of Group III revealed degeneration of mitochondria, these changes became worse with prolonged duration of exposure. This toxic effect of acrylamide could be minimized when Vitamin E is given concomitantly with it. Conclusion: Acrylamide lead to histological changes in rat tongue. Vitamin E minimized this changes due to its antioxidant effect.

PROTECTIVE EFFECT OF SWIMMING EXERCISE ON ACRYLAMIDE INDUCED DIAPHRAGMATIC MYOPATHY IN MALE ALBINO RATS

Background: Acrylamide (ACR) naturally forms during high-temperature cooking of food. Many studies concluded that ACR has neurological, reproductive toxicities, and can produce carcinogenesis. However, the toxic effect of acrylamide on diaphragmatic muscle is not fully investigated. Objective: To evaluate the effect of acrylamide on diaphragmatic muscle and the effect of swimming exercise on diaphragmatic muscle after exposure to acrylamide. Materials and methods: Thirty white male albino rats classified into three groups, control, acrylamide, and (swimming & acrylamide) groups. Muscle enzymes were assayed. The diaphragm was weighed, and diaphragmatic muscle contractions were recorded and assessed histologically. Results: Acrylamide group significantly increased Creatine kinase-MB (CK-MB) and LDH insignificantly while Troponin I and T decreased. Acrylamide increased Malondialdehyde (MDA) and decreased Superoxide dismutase (SOD). Swimming exercise with acrylamide increased LDH, SOD, decreased Troponin I and T and MDA. Acrylamide increased diaphragmatic muscle weight and decreased muscle contraction immediately and after 30 minutes of activity, swimming exercise returned the weight of the muscle near to normal and increased contractions. Histologically, acrylamide group showed degeneration, splitting, fatty and cellular infiltration, dilatation and hemorrhage of the blood vessel, reduction of glycogen and decrease expression of desmin. Swimming exercise improved the histological architecture of the diaphragmatic muscle, increased glycogen content and the expression of desmin. Conclusion: Acrylamide induced muscle myopathy by oxidative stress, muscle dystrophy, reduction of glycogen content and decreased desmin expression with reduction of diaphragmatic muscle contraction. Swimming exercise ameliorated the effect of acrylamide on diaphragmatic muscle by reversing the previous undesired effects of acrylamide.

Ecotoxicological Analysis of Acrylamide Using a Microalga as an Indicator Organism

Aquatic ecosystems are very prone to contamination. The fast and accurate assessment of the toxicity of water is an important tool for environmental safety. The aim of this study was to assess the possible toxic effects of acrylamide on physiological parameters of the Chlorophyceae Desmodesmus quadricauda. Cells in exponential growth phase were exposed for 72 h to different concentrations of acrylamide. Light microscopy analysis documented cell density, number of cells per coenobia, cell dimensions, and biovolume; chlorophyll a concentration was also determined. Result show that EC50 of acrylamide for D. quadricauda is 5.88 mg/L. Significant morphological changes were also observed for phenotypic plasticity and cellular dimensions. The most noticeable changes were the significant increase in one-celled coenobia over 24 and 48 h of exposure to EC50. These findings demonstrate that acrylamide may affect aquatic life, not only through growth inhibition, but also inducing phenotypic plasticity and also be problematic when used in high concentrations for water supply.

Toxic effect of acrylamide on the development of hippocampal neurons of weaning rats

Although numerous studies have examined the neurotoxicity of acrylamide in adult animals, the effects on neuronal development in the embryonic and lactational periods are largely unknown. Thus, we examined the toxicity of acrylamide on neuronal development in the hippocampus of fetal rats during pregnancy. Sprague-Dawley rats were mated with male rats at a 1:1 ratio. Rats were administered 0, 5, 10 or 20 mg/kg acrylamide intragastrically from embryonic days 6-21. The gait scores were examined in pregnant rats in each group to analyze maternal toxicity. Eight weaning rats from each group were also euthanized on postnatal day 21 for follow-up studies. Nissl staining was used to observe histological change in the hippocampus. Immunohistochemistry was conducted to observe the condition of neurites, including dendrites and axons. Western blot assay was used to measure the expression levels of the specific nerve axon membrane protein, growth associated protein 43, and the presynaptic vesicle membrane specific protein, synaptophysin. The gait scores of gravid rats significantly increased, suggesting that acrylamide induced maternal motor dysfunction. The number of neurons, as well as expression of growth associated protein 43 and synaptophysin, was reduced with increasing acrylamide dose in postnatal day 21 weaning rats. These data suggest that acrylamide exerts dose-dependent toxic effects on the growth and development of hippocampal neurons of weaning rats.

Glycidamide inhibits progesterone production through reactive oxygen species-induced apoptosis in R2C Rat Leydig Cells

The food contaminant acrylamide (AA) is usually recognized as a probable human carcinogen. In addition, AA has also been found able to induce male infertility in animals. Interestingly, resent research work revealed that the toxic effect of AA on the ability of male reproduction in vivo may due to glycidamide (GA) which is the metabolite of AA. In this study, R2C Leydig cells was used to investigate the toxic effects of GA on progesterone production. GA caused dose-dependent inhibition on the cell growth, with IC25, IC50, and IC75 values found at 0.635, 0.872, and 1.198 mM, respectively. The results of single cell gel/Comet assay showed that GA significantly induced early-phase cell apoptosis, reduced progesterone production, as well as decreasing the protein expression of steroidogenic acute regulatory (StAR) in R2C cells. Furthermore, GA induced overproduction of intracellular reactive oxygen species (ROS), upregulated Bax expression, decreased mitochondrial membrane potential, and triggered mitochondria-mediated cell apoptosis. Consequently, the downstream effector caspase-3 was activated, resulting in Leydig cells apoptosis. Overall, our results showed that GA could damage R2C Leydig cells by the lesion of the ability of progesterone genesis and inducing cells apoptosis.

The antagonistic effect and mechanism of N-acetylcysteine on acrylamide-induced hepatic and renal toxicity

The aim of this study is to investigate hepatic and renal toxicity of acrylamide (ACR) , the antagonistic effect and possible mechanism of N-acetylcysteine (NAC) on the toxicity. Forty female SD rats were randomly divided into four groups. All the rats were administrated by intraperitoneal(i.p.) injection and 1.5 hours later by gavage. The control group was administrated with 0.9% NaCl by i.p. injection and gavaged with 0.9% NaCl. The NAC group was administrated with 200 mg/kg NAC by injection and gavaged with 0.9% NaCl. The ACR group was administrated with 0.9% NaCl by injection and gavaged with 40 mg/kg ACR. The combined treatment group was administrated with 200 mg/kg NAC by i.p. injection and gavaged with 40 mg/kg ACR. The rats were administrated once a day for 2 weeks. After 24 hours of the last administration, the rats were decapitated. The blood was collected, the liver and kidney were separated. The body weight, organ coefficient and serum biochemical parameters were measured, and the pathological changes of the tissues were examined with a microscope. Then the expression of NF-κB p65, IκB-α and COX-2 were detected by Western blot. From the second day to the end of the exposure, the body weight of rats in the ACR group was statistically lower than that in the control group (P<0.05) . Compared with the combined treatment group, the body weight in the ACR group statistically decreased in the second and third days (P < 0.05) . The liver and kidney organ coefficients in the ACR group were (4.159%±.371%) and (0.764%±0.068%) respectively, which increased statistically when compared with the control group (P < 0.05) . The contents of ALT, AST and Cr in the serum in the ACR group were (77.370±16.397) U/L、(379.410±57.817) U/L and (77.812±6.391) μmol/L respectively, which were not significantly different with those in the control group and the combined treatment group (P>0.05) . The content of BUN in the serum in the ACR group was (7.005±1.009) mmol/L, which was statistically higher than that in the control group (P<0.05) . Histopathology results showed unclear boundary and nucleus pyknosis in hepatocytes, loose and disordered structures of hepatic cords in the ACR group, but no obvious pathology changes were observed in the kidneys of each group. In the Western blot results, the expression of nuclear NF-κB p65 and COX-2 in the liver in the ACR group was statistically higher than that in the control group and the combined treatment group (P<0.05) , and the expression of IκB-α in the liver in the ACR group statistically decreased compared with the control group and the combined treatment group (P<0.05) . The expression of total NF-κB p65 in the liver in the ACR group was statistically higher than that in the control group (P<0.05) . Under the conditions of this experiment, ACR may induce hepatic toxicity through the activation of NF-κB signaling pathway, and NAC could antagonize the hepatic toxicity of ACR by inhibiting the NF-κB signaling pathway, whereas the toxic effect of ACR on kidney needs to be further studied.

Influence of acrylamide on the gastric mucosa of adult albino rats and the possible protective role of rosemary.

Acrylamide is a common chemical found in heated starchy foods especially potato products. We investigated, for the first time, the effect of acrylamide, alone or with rosemary, on the structure of gastric mucosa of adult male albino rats. Stomach sections were examined using light and scanning electron microscopy. Quantitative immmunohistochemical assessments of the expression of caspase-3, inducible NO synthase (iNOS) and epidermal growth factor receptor (EPGR) were performed. Our results showed that acrylamide produced mucosal erosions and depletion of the protective surface mucus together with widespread inflammatory infiltration. In addition, there was significantly increased expression of caspase-3 and iNOS and weak expression of EPGR. Rosemary exerted a protective effect against acrylamide-induced gastric toxicity via reducing oxidative stress, apoptosis and inflammation as well as accelerating the healing process. The results of this work add to the known toxic effects of acrylamide and provide a new insight into the possible use of rosemary to ameliorate these effects.

The impact of vitamin E against acrylamide induced toxicity on skeletal muscles of adult male albino rat tongue: Light and electron microscopic study

Acrylamide, one of the major environmental public health problems, results from its increased accumulation in the process of cooking food materials. This study aimed to demonstrate the light and electron microscopic structural effects of acrylamide on the skeletal muscle fibers of adult male albino rat tongue and to investigate the possible protective effect of vitamin E co-administration. Thirty adult male albino Sprague–Dawley rats were divided into 3 groups, each group included 10 rats. Group I (control), group II which was subdivided into two equal subgroups: subgroup IIa: included 5 rats that received acrylamide orally once daily for 20 days. Subgroup IIb: included 5 rats that received acrylamide orally once daily for 40 days. Group III was also subdivided into two equal subgroups: subgroup IIIa: included 5 rats that received acrylamide and vitamin E orally once daily for 20 days. Subgroup IIIb: included 5 rats that received acrylamide and vitamin E orally once daily for 40 days. At the end of the experiment the tongue was dissected out for histological and electron microscopic studies, another muscle sample was homogenized and processed for biochemical estimation of malondialdehyde (MDA) and total antioxidant capacity (TAC). Light microscopic study of tongue skeletal muscles in acrylamide exposed animals revealed abnormal wavy course and splitting of the muscle fibers with fatty infiltration in between. Moreover, pyknosis and remnants of nuclei were detected. EM revealed marked aggregation of mitochondria of different size and shape with giant cells formation, and partial loss of myofilaments. There were statistically significant increase in MDA and decrease in TAC indicating oxidative stress in acrylamide administrated groups (group II) than the control group which increased by prolonged duration (subgroup IIb versus subgroup IIa, p<0.0001). This oxidative stress could explain the histological changes in tongue muscles of acrylamide exposed rats. Co-administration of vitamin E with acrylamide ameliorated most of the above mentioned histological changes in the animals used and signs of improvement that became better with prolonged administration of it (subgroup IIIb versus subgroup IIIa, p<0.0001) were detected. It could be concluded that, chronic exposure to acrylamide might lead to skeletal muscle damage in rat tongue which becomes worth with prolonged duration of exposure. Acrylamide induced oxidative stress is the implicated mechanism of such histological changes. This toxic effect of acrylamide could be minimized when vitamin E is given concomitantly with it by its antioxidant effect.

Dietary levels of acrylamide affect rat cardiomyocyte properties

The toxic effects of acrylamide on cytoskeletal integrity and ion channel balance is well-established in many cell types, but there has been little examination regarding the effects of acrylamide on primary cardiomyocytes, despite the importance of such components in their function. Furthermore, acrylamide toxicity is generally examined using concentrations higher than those found in vivo under starch-rich diets. Accordingly, we sought to characterize the dose-dependent effects of acrylamide on various properties, including cell morphology, contraction patterns, and junctional connexin 43 staining, in primary cardiomyocytes. We show that several days exposure to 1–100μM acrylamide resulted in altered morphology, irregular contraction patterns, and an increase in the amount of immunoreactive signal for connexin 43 at cell junctions. We conclude that dietary levels of acrylamide may alter cellular function with prolonged exposure, in primary cardiomyocytes.

Camellia sinensis (green tea) extract attenuate acrylamide induced testicular damage in albino rats

Acrylamide is a proved toxin for testicular function, found in food when heated for long period of time. Green tea (Camellia sinensis) is a potent antioxidant; the aim of this study was to investigate the protective effect of green tea extract against the toxic effects of acrylamide in rat testes. acrylamide was administered orally to rats in different doses and also the extract of green tea was administered orally to different groups of animals in combination with the acrylamide. The weight of animals, testosterone hormone level and histopathological effect upon testicles were evaluated. Testosterone hormone level in serum, and histopathological findings were significantly improved with the co-administration of green tea extract with the acrylamide. Green tea extract reversed all the toxic effects of acrylamide even in high dose for long period (90 days). Green tea extract is a potent antioxidant antidote for the acrylamide toxic effects upon testicular function.

Effect of sub-acute exposure to acrylamide on GABAergic neurons and astrocytes in weaning rat cerebellum

Occupational exposure and experimental intoxication of acrylamide (ACR) can produce skeletal muscle weakness and ataxia. In this study, we tested whether ACR would affect cerebellar function through the regulation of gamma-aminobutyric acid (GABA) and glial fibrillary acidic protein (GFAP) expression in cerebellum. Weaning male Sprague-Dawley rats were gavaged with ACR (5, 15, 30 mg/kg, 5 days per week) or saline for 4 weeks. Effects of ACR on the cerebellum were observed. For the 5 mg/kg group, no obvious change was observed, whereas moderate and severe ataxia were observed in the 15 mg/kg and 30 mg/kg groups, respectively. For the 15 mg/kg and 30 mg/kg groups, cerebellum concentrations of glutamate and GABA were dose-dependently decreased and increased, respectively. Moreover, the expression of GABA, the GABAergic presynaptic marker glutamate acid decarboxylase-65 (GAD65) and GFAP were significantly increased in those 2 groups. The results suggested that weaning rats were sensitive to ACR and that the toxic effects of ACR on the cerebellum may be associated with the increased expression of GABA and reactive astrocytes hypertrophy.

Toxicological effects of acrylamide on the reproductive system of weaning male rats

It has been reported that acrylamide can be detected in starchy food treated by high temperature (120 °C). People could be exposed to acrylamide in factory, laboratory, or even in daily life via diet and drinking water. Recently, the toxicity of acrylamide receives more attention. In addition to the neurotoxicity in humans, other toxic effects of acrylamide are worth further investigation. In this study, we investigated whether acrylamide affected the male reproductive system using high-performance liquid chromatography. In this study, the reproductive toxicity of acrylamide was observed in 3-week-old weaning male Sprague-Dawley rats treated with acrylamide at various doses (0, 5, 15 or 30 mg/kg/day). The results showed that food availability and reproductive organ indexes of the weaning male rats decreased. Levels of follicle-stimulating hormone and testosterone in serum increased while luteinizing hormone in serum decreased. The histopathological lesions and abnormal sperms presented in weaning rats after acrylamide treatment. The results suggested that there is a toxicological effect of acrylamide on the reproductive system of weaning male rats. Based on the findings above, we suggested that more attention should be paid to the toxicological study of acrylamide on weaning male rats or human beings, rather than just on adult male animals.

Evaluation of the Antitoxic Effect of Phthalides from Apium graveolens in Acrylamide Intoxication I. Evolution of the Hepatic Cytolysis and Proteosynthetic Parameters in Acrylamide Intoxication on the Background of Phthalide Protection

Acrylamide is a toxic compound formed during thermical processing of foods that contain amino acids, mainly asparagine, and reducing sugars. The toxicodynamics of acrylamide, exerted mainly by its major metabolite glycidamide, is expressed by mutagenic, carcinogenic and imunosupressive effects. Due to its toxicity and its high prevalence in aliments, the present paper approaches a possible way of reducing the toxic effects of acrylamide by using phytotherapeutical means. In this direction, the antitoxic potential of some phytopreparates obtained from Apium graveolens (Apii aetheroleum, extractive solutions from A. radix, A. folium and A. semen) were monitorized on the background of acrylamide intoxication. The antitoxic potential of phthalides has been evaluated by determining biochemical parameters: hepatic cytolysis parameters (aspartate aminotransferase, alanil aminotransferase, lactate dehydrogenase) and protesosynthesis parameters (colinesterase, total poteins, albumins). The biochemical investigation confirmed the antitoxic potential fo phthalides from celery, the highest protection being obtained for the phytopreparate from Apii semen.