Acrylamide Intoxication Research Articles

Protective effect of rutin on acrylamide induced ovarian inflammation, oxidative stress, DNA damage, and hormonal changes: Based on in silico and in vivo study.

Acrylamide (AA) is a carcinogenic compound that affects people due to its frequent use in laboratories and industry as well as the high-temperature cooking of foods with high hydrocarbon content. AA is known to cause severe reproductive abnormalities. The main aim of this study is to evaluate the protective effect of rutin (RU), a phytoactive compound, against AA-induced reproductive toxicity in female rats. Initially, rats were exposed to AA (40 mg/kg for 10 days). Therapy of RU was given after AA intoxication consecutively for 3 days. After 24 h of the last treatment, all the animals were sacrificed. The study evaluated reproductive hormones, oxidative stress markers, membrane-bound enzymes, DNA damage, histological findings, and an in silico approach to determine the protective efficacy of RU. The results indicated that RU significantly protected against inflammation, oxidative stress, and DNA damage induced by AA, likely due to its antioxidant properties.

Morphological changes in the liver parenchyma in rats under subacute acrylamide intoxication and the possibility of their preventive treatment

Introduction. Acrylamide, used in industry, is also formed in foods during high temperature processing. Acrylamide has a toxic effect on the nervous, reproductive, and other systems of the body, due to carcinogenic and genotoxic properties. Considering sufficiently serious threat of acrylamide to human health, it is relevant to carry out further fundamental research to study the mechanism of its impact on the body and the possibility of treatment of lesions caused by it.
 The aims of this study is to assess morphological changes in the liver of experimental animals under acute acrylamide intoxication and study the possibility of their preventive treatment with complex compounds based on oxymethyluracil.
 Materials and methods. Experimental studies on the subacute effects of acrylamide at a dose of 20 mg/kg on the histological structure of the liver were carried out on outbred female rats. The efficiency of preventive administration of complex compounds of oxymethyluracil with ascorbic acid, with sodium succinate and acetylcysteine ​​was also studied.
 Results. Exposure to acrylamide for 28 days at a dose of 20 mg/kg of body weight in experimental rats, has been established to cause minor morphological changes in the structure of the liver: only focal cellular infiltrates were found in the centrilobular zones. In groups of rats that received preventive treatment with complex compounds based on oxymethyluracil, no formation of infiltrates and other pathological changes was observed.
 Limitations. Limitations of the study are related to implementation of experimental studies of the pathomorphological changes in the liver of experimental animals using only one dose of acrylamide - 20 mg per kg of body weight during one limited period (28 days).
 Conclusion. Exposure to acrylamide for 28 days at a dose of 20 mg/kg of body weight causes minor morphological changes in the structure of the liver in experimental rats. For the first time, the effectiveness of prophylactic correction of the toxic effect of acrylamide with complex compounds of oxymethyluracil with ascorbic acid, sodium succinate and acetylcysteine, which showed a certain protective effect on the liver, was studied.

Acrylamide interferes with autophagy and induces apoptosis in Neuro-2a cells by interfering with TFEB-regulated lysosomal function.

Acrylamide (ACR), a well-documented human neurotoxicant that is widely exists in starchy foods. More than 30% of human daily energy is provided by ACR-containing foods. Evidence indicated that ACR can induce apoptosis and inhibit autophagy, but the mechanisms are limited. Transcription Factor EB (TFEB) is a major transcriptional regulator of the autophagy-lysosomal biogenesis that regulates autophagy processes and cell degradation. Our study aimed to investigated the potential mechanisms of TFEB-regulated lysosomal function in ACR-caused autophagic flux inhibition and apoptosis in Neuro-2a cells. Our results found that ACR exposure inhibited the autophagic flux, as revealed by the elevated LC3-II/LC3-I and p62 levels and a notable increased autophagosomes. ACR exposure reduced the amounts of LAMP1 and mature cathepsin D and caused an accumulation of ubiquitinated proteins, which suggests lysosomal dysfunction. In addition, ACR increased cellular apoptosis via decreasing Bcl-2 expression, increasing Bax and cleaved caspase-3 expression, and raising the apoptotic rate. Interestingly, TFEB overexpression alleviated the ACR-induced lysosomal dysfunction, and then mitigated the autophagy flux inhibition and cellular apoptosis. On the other hand, TFEB knockdown exacerbated the ACR-induced lysosomal dysfunction, autophagy flux inhibition, and cellular apoptosis. These findings strongly suggested that TFEB- regulated lysosomal function is responsible for ACR-caused autophagic flux inhibition and apoptosis in Neuro-2a cells. The present study hopes to explore new sensitive indicators in the mechanism of ACR neurotoxicity and thus provide new targets for the prevention and treatment of ACR intoxication.

Mitophagy suppresses motor neuron necroptotic mitochondrial damage and alleviates necroptosis that converges to SARM1 in acrylamide-induced dying-back neuropathy.

Acrylamide (ACR), a common industrial ingredient that is also found in many foodstuffs, induces dying-back neuropathy in humans and animals. However, the mechanisms remain poorly understood. Sterile alpha and toll/interleukin 1 receptor motif-containing protein 1 (SARM1) is the central determinant of axonal degeneration and has crosstalk with different cell death programs to determine neuronal survival. Herein, we illustrated the role of SARM1 in ACR-induced dying-back neuropathy. We further demonstrated the upstream programmed cell death mechanism of this SARM1-dependent process. Spinal cord motor neurons that were induced to overexpress SARM1 underwent necroptosis rather than apoptosis in ACR neuropathy. Mechanically, non-canonical necroptotic pathways mediated mitochondrial permeability transition pore (mPTP) opening, reactive oxygen species (ROS) production, and mitochondrial fission. What's more, the final executioner of necroptosis, phosphorylation-activated mixed lineage kinase domain-like protein (MLKL), aggregated in mitochondrial fractions. Rapamycin intervention removed the impaired mitochondria, inhibited necroptosis for axon maintenance and neuronal survival, and alleviated ACR neuropathy. Our work clarified the functional links among mitophagy, necroptosis, and SARM1-dependent axonal destruction during ACR intoxication, providing novel therapeutic targets for dying-back neuropathies.

English

When many widely ingested foods are heated, a toxin called acrylamide (ACR) is created. The aim of our research was to investigate if N acetylcysteine (NAC) and/or vitamin E (Vit E) could provide protection against neurotoxicity induced by ACR. Rats were classified into seven groups of 7 rats; control (saline); NAC (150 mg/kg bw); Vit E (100 mg/kg bw); ACR (20 mg/kg bw orally); ACR+NAC; ACR+Vit E; ACR+NAC+Vit E. Saline, NAC and/or Vit E were administered orally, once daily for 30 days. Acetylcholinesterase (AChE) inhibition, glutathione depletion, and elevated levels of malondialdehyde (MDA), were all observed after ACR intoxication. Furthermore, ACR diminished superoxide dismutase (SOD) and catalase (CAT) activities, as well as inflammatory mediators as interleukins (IL-1, IL-6), and tumor necrosis factor-α (TNF-α). The combined treatment of ACR with NAC or Vit E dramatically reduced both oxidative and biochemical consequences, with a more frequent return to normal values. To conclude, NAC or Vit E supplementation may alleviate ACR-induced neuronal injury, most likely due to NAC or Vit E antioxidant, anti-inflammatory, and anti-apoptotic effects

Attenuating effect of Chlorella Vulgaris against acrylamide intoxication on thyroid gland

Oral administration of Acrylamide in our food produces adverse health effects through different vital systems. This study examined the effect of simultaneous oral supplementation of unicellular algae Chlorella vulgaris (CV) on thyroid gland disruption induced by intoxication with Acrylamide (ACR). Healthy male rats (n=60) distributed in six groups: -ve control, +ve control (CV 300 mg/kg), low dose Acrylamide (LACR, 5 mg/kg), high dose Acrylamide (HACR, 50 mg/kg), pre-administration of Chlorella Vulgaris with Acrylamide CV+ LACR (5mg/kg), and with Acrylamide CV+HACR (50 mg/kg). All groups received treatments orally for 30 days. ACR treated groups (LACR, HACR) demonstrated a significant elevation in oxidative stress biomarkers Malondialdehyde (MDA), 4-Hydroxynonenal (4-HNE), Nitric Oxide (NO) and pro-inflammatory cytokines C-reactive protein (CRP), Tumor Necrosis Factor alpha (TNF-α), Interleukin 6 (IL-6) and Interleukin 1 beta (IL-1β). In relation to antioxidant biomarkers Glutathione (GSH) and Glutathione peroxidase (GPx), GSH recorded significant reduction while GPx indicated significant elevation as compared to control and +ve control group at (p<0.05). Thyroid gland biomarkers showed reduction in Thyroid-Stimulating hormone (TSH) in ACR groups whereas Thyroxine (T4) and Triiodothyronine (T3) presented a significant elevation.

Administration of Different Doses of Acrylamide Changed the Chemical Coding of Enteric Neurons in the Jejunum in Gilts.

Excessive consumption of highly processed foods, such as chips, crisps, biscuits and coffee, exposes the human to different doses of acrylamide. This chemical compound has a multidirectional, adverse effect on human and animal health, including the central and peripheral nervous systems. In this study, we examined the effect of different doses of acrylamide on the enteric nervous system (ENS) of the porcine jejunum. Namely, we took into account the quantitative changes of neurons located in the jejunum wall expressing substance P (SP), galanin (GAL), a neuronal form of nitric oxide synthase (nNOS), the vesicular acetylcholine transporter (VAChT) and cocaine- and amphetamine-regulated transcript (CART). The obtained results indicate that acrylamide causes a statistically significant increase in the number of neurons immunoreactive to SP, GAL, VAChT and CART in all types of examined enteric plexuses and a significant drop in the population of nNOS-positive enteric neurons. Changes were significantly greater in the case of a high dose of acrylamide intoxication. Our results indicate that acrylamide is not indifferent to ENS neurons. A 28-day intoxication with this substance caused marked changes in the chemical coding of ENS neurons in the porcine jejunum.

The therapeutic potential of berberine chloride against SARM1-dependent axon degeneration in acrylamide-induced neuropathy.

Chronic acrylamide (ACR) intoxication causes typical pathology of axon degeneration. Moreover, sterile-α and toll/interleukin 1 receptor motif-containing protein 1 (SARM1), the central executioner of the programmed axonal destruction process under various insults, is up-regulated in ACR neuropathy. However, it remains unclear whether inhibitors targeting SARM1 are effective or not. Among all the pharmacological antagonists, berberine chloride (BBE), a natural phytochemical and the first identified non-competitive inhibitor of SARM1, attracts tremendous attention. Here, we observed the protection of 100 μM BBE against ACR-induced neurites injury (2 mM ACR, 24 hr) in vitro, and further evaluated the neuroprotective effect of BBE (100 mg/kg p.o. three times a week for 4 weeks) in ACR-intoxicated rats (40 mg/kg i.p. three times a week for 4 weeks). The expression of SARM1 was also detected. BBE intervention significantly inhibited the overexpression of SARM1, ameliorated axonal degeneration, alleviated pathological changes in the sciatic nerve and spinal cord, and improved neurobehavioral symptoms in ACR-poisoned rats. Thus, BBE exhibits a strong neuroprotective effect against the SARM1-dependent axon destruction in ACR neuropathy. Meanwhile, our study underscores the need for appropriate inhibitor selection in diverse situations that would benefit from blocking the SARM1-dependent axonal destruction pathway.

Protective Effects of Wine Polyphenols on Oxidative Stress and Hepatotoxicity Induced by Acrylamide in Rats.

In recent years, it has been increasingly suggested that the consumption of natural polyphenols, in moderate amounts, is beneficial for health. The aim of this study was to investigate the efficacy of a red wine (the administered dose of 7 mL/kg/day being equivalent to ~16.5 mg/kg/day total polyphenols) compared to a white wine (the administered dose of 7 mL/kg/day being equivalent to ~1.7 mg/kg/day total polyphenols), on the prevention of acrylamide-induced subacute hepatic injury and oxidative stress in Wistar rats. Hepatic damage due to acrylamide intoxication (the administered dose being 250 µg/kg body weight, for 28 days, by intragastric gavage) was assessed by employing biochemical parameters (aspartate aminotransferase (AST) and alanine aminotransferase (ALT)) and by histopathological studies. Markers of oxidative damage were measured in terms of plasma malondialdehyde (MDA), hepatic Thiobarbituric Acid Reactive Substances (TBARS) and glutathione (GSH) levels, and liver antioxidant enzyme (superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPx)) activities. Regarding hepatic enzyme activities, treatment with red wine significantly decreased the AST values (p < 0.05), while for the ALT values only a normalization tendency was observed. Treatment with red wine and white wine, respectively, significantly prevented the increase in MDA and TBARS levels (p < 0.05), as well as the depletion of GSH (p < 0.05). Red wine treatment normalized the activities of the antioxidant enzymes CAT and SOD in rats intoxicated with acrylamide, while supplementing the diet with white wine did not produce significant differences in the antioxidant enzyme activities. Histopathological findings revealed a moderate protective effect of red wine after four weeks of daily consumption. Our findings provide evidence that red wine, having a higher phenolic content than white wine, has a significant protective effect on oxidative stress and liver injury induced by acrylamide in rats, through its antioxidative activity.

The potential neuroprotective effect of allicin and melatonin in acrylamide-induced brain damage in rats.

Acrylamide (ACR) is an unsaturated monomer that served various fields; however, it is a potent neurotoxin. The target of the present study is to explore the neuroprotective efficacy of allicin and melatonin on ACR-induced neurotoxicity. Thirty-six male adult rats were non-selectively separated into six groups: placebo, allicin (20 mg/kg b.w daily per os), melatonin (10 mg/kg b.w 3 times/week per os), ACR (50 mg/kg b.w daily per os), ACR-allicin, and ACR-melatonin at the same doses as the preceding groups. The assessment of brain biomarkers, neurotransmitters, antioxidative status, Nrf2 signaling pathway, and histopathological analyses was performed following 21 days. ACR exposure induced brain lipid and DNA oxidative damage as well as reduced the glutathione (GSH) levels. The obvious brain oxidative injuries contributed to distinct brain dysfunction that was assured by alteration of brain neurotransmitters (serotonin, dopamine, acetylcholine, and acetylcholinesterase) and pathological brain lesions. Furthermore, ACR exposure increased hydroxy deoxyguanosine (8-OHdG), tumor necrosis factor-α (TNF-α), and amyloid protein (AB1-42). Finally, the mRNA transcripts of brain Keap-1, Nrf2, and NF-kB were upregulated after ACR intoxication. Interestingly, allicin and melatonin alleviated the ACR-induced brain damage assessed by the normalization of the mentioned analyses. The present study demonstrated the protective role of both allicin and melatonin in ACR-prompted neuropathy by alleviation of redox imbalance and enhancement of neurotransmitters as well as relieving DNA damage and anti-inflammatory effect.

Protective effects of thymoquinone against acrylamide-induced liver, kidney and brain oxidative damage in rats.

Acrylamide (AA), an industrial monomer, may cause multi-organ toxicity through induction of oxidative stress and inflammation. The antioxidant properties of thymoquinone (TQ), an active constituent of Nigella sativa, have been established before. The aim of the current study was to assess the protective effects of TQ against AA-induced toxicity in rats. Forty-eight male Wistar rats were divided into six groups each of eight rats. The first group acted as a negative control and received normal saline. Groups II and III were administered TQ orally at doses of 10 and 20 mg/kg b.wt., respectively, for 21 days. The four group received AA (20 mg/kg b.wt.) for 14 days. The five and six groups were given TQ at either dose for 21 days, starting seven days before AA supplementation (for 14 days). Acrylamide intoxication was associated with significant (p < 0.05) increases in serum levels of liver injury biomarkers (alanine transferase, aspartate transferase, and alkaline phosphatase), renal function products (urea, creatinine), DNA oxidative damage biomarker (8-oxo-2'-deoxyguanosine), and pro-inflammatory biomarkers (interleukin-1β, interleukin-6, and tumor necrosis factor-α). Moreover, AA intoxication was associated with increased lipid peroxidation and nitric oxide levels, while reduced glutathione concentration and activities of glutathione peroxidase, superoxide dismutase, and catalase in the liver, kidney, and brain. TQ administration normalized AA-induced changes in most serum parameters and enhanced the antioxidant capacity in the liver, kidney, and brain tissues in a dose-dependent manner. In conclusion, the current experiment showed that TQ exerted protective and antioxidant activities against AA-induced toxicity in mice.

Effect of Acrylamide Supplementation on the CART-, VAChT-, and nNOS-Immunoreactive Nervous Structures in the Porcine Stomach.

Simple SummaryThe progress of civilization has provided people with virtually unlimited access to food products. However, while the pace of life has increased, the consumption of products with high levels of acrylamide (e.g., chips, corn flakes or coffee) has also increased. The gastrointestinal tract is the first-exposure site for noxious substances ingested with food and it is also often the first defence mechanism. Changes in the expression of neuroactive substances in the intramural neurons of the enteric nervous system (ENS) are a common preclinical symptom of the harmful effect of pathological factors on the body. Using the double immunofluorescence staining method, it was established that supplementation with low and high doses of acrylamide resulted in alterations of the porcine stomach neuron phenotype, which was reflected in an increased number of the cocaine- and amphetamine-regulated transcript (CART)-, vesicular acetylcholine transporter (VAChT)-, and neuronal isoform of nitric oxide synthase (nNOS)-immunoreactive neurons. The recorded changes revealed that even low doses of acrylamide influence the nervous structures located in the porcine gastric wall. This may result from the neurotoxicity of acrylamide or from the response of the ENS to acrylamide-induced inflammation and suggests an important role of the ENS in protecting the gastrointestinal tract during acrylamide intoxication.Acrylamide is found in food products manufactured with high-temperature processing, and exposure to acrylamide contained in food products may cause a potential risk to human health. The aim of this investigation was to demonstrate the changes in the population of CART-, nNOS-, and VAChT-immunoreactive enteric neurons in the porcine stomach in response to supplementation of low and high acrylamide doses. The study was carried out with 15 Danish landrace gilts divided into three experimental groups: the control group—animals were administered empty gelatine capsules; the low-dose group—animals were administrated a tolerable daily intake (TDI) dose (0.5 µg/kg of body weight (b.w.)/day) of acrylamide capsules, and the high-dose group—animals were administrated high-dose (ten times higher than TDI: 5 µg/kg b.w./day) acrylamide capsules for 28 days. Using the double immunofluorescence staining method, it was established that supplementation with low and high doses of acrylamide resulted in alterations of the porcine stomach neuron phenotype, which was reflected in an increased number of CART-, VAChT-, and nNOS-immunoreactive neurons. These changes were accompanied by an increased density of CART-, VAChT-, and nNOS-positive fibres. The results suggest that the enteric nervous system plays an important role in protecting the gastrointestinal tract during acrylamide intoxication.

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.

Diosmin protects against acrylamide-induced toxicity in rats: Roles of oxidative stress and inflammation

Acrylamide (ACR) is a toxic substance produced by oxidative stress. The recent study focused on stimulation of ACR through ROS intracellular production thereby playing a crucial aspect in the process of toxicity. This is positioned on a relevant research and study on the antioxidant characteristics of diosmin. This research was shown to examine the shielded effect of diosmin against ACR toxicity. Forty rats (male) were grouped in five categories. The control category was given normal saline followed by the second category which was given diosmin (100 mg/kg b.wt oral administered). The next category was given ACR (30 mg/kg b.wt orally) every day for 14 days. The fourth and fifth groups were supplemented by acrylamide (30 mg/kg b.wt) after diosmin given orally (at 50 or 100 mg/kg b.wt for 7days). Upon examination of the specimens over a period of the given time frame, it was found that acrylamide intoxication remarkably rising levels of serum (aspartate transferase, alanine transferase, ALP, urea, creatinine, interleukin 1 beta ,and interleukin 6. Besides, it increased the brain, hepatic and renal lipid peroxidation, at the same time, weakening the antioxidant biomarkers accumulation and activities. The introduction of diosmin also alleviated the serum aspartate transferase, alanine transferase, APL, urea, creatinine, as well as plasma pro-inflammatory cytokines such as interleukin-1-beta and interleukin-6. Further to this, both diosmin doses remarkably lowered the levels of MAD in the tissues and nitric oxide which further increased the glutathione, glutathione peroxidase, superoxide dismutase, and catalase, in contrast to the ACR-injected group. Based on these findings, administered diosmin standardized the modified serum framework, halted the peroxidation, and magnified the accumulation and working effects of the biomarker antioxidants in the brain, hepatic and renal tissues of the rats in the current dose-dependent research. Therefore, these findings show that diosmin has a protective reaction in defiance to the toxicity produced by acrylamide through the free radical scavengers along with potent antioxidant occurrences.

Protective effects of hesperidin and diosmin against acrylamide-induced liver, kidney, and brain oxidative damage in rats.

Acrylamide (AA) is a heat-induced toxin formed during thermal processing of many commonly consumed foods, including meat products, French fries, potato crisps, bread, cereals, cookies, and coffee. There is thus potentially high dietary exposure of humans to AA, which can induce significant oxidative stress. Hesperidin (HS) and diosmin (DS) are flavone glycosides that have antioxidant properties. The aim of this study was to investigate the protective effects of HS and DS against AA toxicity. Fifty-six adult male Wistar albino rats were divided into seven groups. The first group was orally administered 0.5% (w/v) dimethyl sulfoxide (DMSO) and considered as the control group. The second and third groups were orally administered 10 mg/kg/day of HS or DS, respectively. The fourth group received 20 mg/kg/day of AA orally for 14 days. The fifth and sixth groups were given 10 mg/kg/day of HS or DS, respectively, followed by AA. The seventh group was given both HS and DS after AA administration. AA intoxication significantly (p ≤ 0.05) increased serum levels of liver function enzymes (ALT, AST, and ALP), kidney function products (urea and creatinine), oxidative DNA damage marker (OHdG), proinflammatory markers (TNF-α, IL-1β, and IL-6), lipid peroxidation marker (malondialdehyde), and nitric oxide (NO). On the other hand, it significantly (p ≤ 0.05) decreased levels of reduced glutathione (GSH) in the liver, kidney, and brain. The activities of glutathione peroxidase (GSH-Px), superoxide dismutase (SOD), and catalase (CAT) in the liver, kidney, and brain tissues were also reduced. HS and DS supplementation prevented lipid peroxidation, normalized the serum parameters altered by AA, and enhanced the tissue concentrations and activities of antioxidant biomarkers. It could be concluded that HS and DS have potent protective effects against oxidative stress, lipid peroxidation, and DNA damage induced by AA toxicity in rats.

Silymarin Ameliorates Acrylamide-Induced Hyperlipidemic Cardiomyopathy in Male Rats

Acrylamide (AA) is a well-known potent carcinogen and neurotoxin that has been recently linked to atherosclerotic pathogenesis. The present study is aimed at investigating the protective effect of silymarin (SIL) as an antioxidant against AA-induced hyperlipidemic cardiomyopathy in male rats. The obtained results showed that animals exposed to AA exhibited a significant increase in the levels of cardiac serum markers, serum total cholesterol, triglycerides, low-density lipoprotein cholesterol, and very-low-density lipoprotein cholesterol with a significant decrease in high-density lipoprotein cholesterol. Furthermore, AA intoxication significantly increased the malondialdehyde level (a hallmark of lipid peroxidation) and reduced antioxidant enzyme activities (i.e., superoxide dismutase, catalase, and glutathione peroxidase). SIL administration significantly attenuated all these biochemical perturbations in AA-treated rats, except for the decreased high-density lipoprotein cholesterol. Our results were confirmed by histopathological assessment of the myocardium. In conclusion, this study demonstrated a beneficial effect of SIL therapy in the prevention of AA-induced cardiotoxicity by reversing the redox stress and dyslipidemia in experimental animals.

Alterations in Galanin-Like Immunoreactivity in the Enteric Nervous System of the Porcine Stomach Following Acrylamide Supplementation.

In recent years, a significant increase in the consumption of products containing large amounts of acrylamide (e.g., chips, fries, coffee), especially among young people has been noted. The present study was created to establish the impact of acrylamide supplementation, in tolerable daily intake (TDI) dose and a dose ten times higher than TDI, on the population of galanin-like immunoreactive (GAL-LI) stomach neurons in pigs. Additionally, in the present study, the possible functional co-operation of GAL with other neuroactive substances and their role in acrylamide intoxication was investigated. Using double-labelling immunohistochemistry, alterations in the expression of GAL were examined in the porcine stomach enteric neurons after low and high doses of acrylamide supplementation. Generally, upregulation in GAL-LI immunoreactivity in both myenteric and submucous plexuses was noted in all stomach fragments studied. Additionally, the proportion of GAL-expressing cell bodies simultaneously immunoreactive to vasoactive intestinal peptide (VIP), neuronal nitric oxide synthase (nNOS) and cocaine- and amphetamine- regulated transcript peptide (CART) also increased. The results suggest neurotrophic or/and neuroprotective properties of GAL and possible co-operation of GAL with VIP, nNOS, CART in the recovery processes in the stomach enteric nervous system (ENS) neurons following acrylamide intoxication.

Copper (I) Nicotinate complex Abrogates Acrylamide Induced Hepatotoxicity in Male Rats: Biochemical and Histological Studies

This study was conducted as a trail to abrogates acrylamide induced hepatotoxicity in male rats by administration of copper (I) nicotinic acid complex. Animals were divided into 4 groups ;GI: control kept on balanced diet and tap water , GII: Acrylamide group received acrylamide in drinking water (7.5 mg/kg b.w.) for 30 days. GIII: treated with copper (I)-nicotinate complex (400 μg/kg b.w.) after acrylamide intoxication for 30 days and GIV the complex then acrylamide (prophylactic). Results showed significant increase in serum levels of AST, ALT, ALP, GGT and total antioxidant capacity (TAC) in acrylamide group. Moreover a significant increase in tumer markers AFU and TNF-Alpha. while Levels of each of S. total protein and S. albumin were significantly decreased in ACR group compared with control. Histological study showed congestion of central vein in liver section and vacuolation of hepatocytes in ACR group. Anticancer activity using in-vitro cytotoxic assay of Cu (I) Nicotinate complex ; proves the anticancer properties of it comparing with doxorubicin. Treatment with Copper (I)-Nicotinate Complex restored tissue and serological indices concomitantly towards normal levels. These results revealed that Copper (I)-Nicotinate Complex is able to significantly alleviate the hepatotoxicity induced by AA in rats and could be utilized as a potent food additives.

Acrylamide-induced alterations in the cocaine- and amphetamine-regulated peptide transcript (CART)-like immunoreactivity within the enteric nervous system of the porcine small intestines

The main goal of the present study was to determine the influence of low and high doses of acrylamide on CART-like immunoreactivity within the ENS of the porcine small intestines. Investigation was performed on 15 sexually immature female pigs, divided into three groups: control group, where empty gelatin capsules were administered, and two experimental groups, where capsules containing low or high doses of acrylamide were given. After 28days of acrylamide exposure all animals were euthanized with a gradual overdose of anaesthetics. Immediately after euthanasia fragments of the duodenum, jejunum and ileum were collected and fixed. Then, 14μm-thick cryostat sections were processed for routine double-labelling immunofluorescence using primary antisera directed towards a pan neuronal marker — protein gene-product 9.5 (PGP 9.5) and cocaine- and amphetamine-regulated peptide transcript (CART). During the present investigation, CART-LI cell bodies were detected in all types of enteric plexuses of duodenum, jejunum and ileum. Acrylamide intoxication resulted in a significant increase in expression of CART in the intramural neurons of the porcine small intestines, especially in myenteric plexuses. It may suggest participation of CART in neuronal protection and recovery processes within the gut. Moreover, results of the present study suggest that even low doses of acrylamide cause a significant response of ENS neurons.

Taurine attenuates acrylamide-induced apoptosis via a PI3K/AKT-dependent manner.

As a potent neurotoxic agent, acrylamide (ACR) is formed in food processing at higher temperature. Taurine (TAU), a nonessential amino acid, is used to cure neurodegenerative disorders, followed by activation of the phosphatidylinositol 3-kinase/protein kinase B (PI3K/AKT) signaling pathway. In this article, we certified that antiapoptotic efficacy of TAU in vivo and vitro. ACR-treated rats received TAU by drinking water 2 weeks after ACR intoxication. The results showed that in treated rats, TAU alleviated ACR-induced neuronal apoptosis, which was associated with the activation of PI3K/AKT signaling pathway. TAU attenuated apoptosis caused by ACR through observing terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL)-positive cells, measure of protein expression of Bcl-2, Bax, and caspase 3 activity. TAU-induced antiapoptotic effect is PI3K/AKT-dependent, which was proved in ACR-intoxicated ventral spinal cord 4.1 cells in the presence of AKT inhibitor, MK-2206. Therefore, our results demonstrated that TAU-attenuated ACR-induced apoptosis in vivo through a PI3K/AKT-dependent manner provided new sights in the molecular mechanism of TAU protection against ACR-induced neurotoxicity.