Acrylamide ; adverse effects ; analysis ; toxicity ; Food Contamination ; analysis ; prevention & control

Prohibited substances in cosmetics refer to substances which must not be among the raw material ingredients of cosmetic products. These substances are absorbed mostly through skin, as well as via lung and gastrointestinal tract. Polyacrylamide is ubiquitously used in industry and its decomposition residue acrylamide (ACR) easily finds its way into cosmetic products. ACR can either be oxidized to epoxide glycidamide or conjugated with glutathione, hemoglobin or DNA; ultimately it is excreted in urine. ACR causes neurotoxicity, reproductive toxicity and tumors in rodents. Occupational exposure to ACR causes neurotoxicity in humans; however, epidemiological evidence have not unambiguously answered the question of whether ACR exposure can increase cancer risk for humans.
Acrylamide ; metabolism ; pharmacokinetics ; toxicity ; Acrylic Resins ; chemistry ; China ; Cosmetics ; chemistry ; Humans

OBJECTIVETo investigate the toxic and DNA damaging effect of acrylamide (AA) on human keratinocytes and its mechanism.

METHODS(1) After the keratinocyte cell line HaCaT cells were exposed to AA with different concentrations for 44 hours, cell survival rate was detected by MTT method. (2) The effects of DNA damage of exposed cells were detected by comet assay. (3) After treating the cells with 2.00 mmol/L of AA plus 0.50 mmol/L of 1-aminobenzotriazole (1-ABT), an inhibitor of cytochrome P-450 enzymes (CYP-450), for 4 hours, the relationship between DNA damage and CYP-450 was studied.

RESULTS(1) Cytotoxicity measurement of AA showed that cell survival rate decreased significantly after 44-hour treatment. (2) Cytotoxicity was not detected after 4-hour AA treatment, but significant DNA damage was observed in all treatment groups, and the degree of damage increased with the concentration of AA. Moreover, the tail lengths of comet cells were in dose-effect relationship. As for cells treated by 1-ABT with 2 mmol/L AA, comet rate and tail length were 15.4% and (8.2 +/- 2.0) micro m respectively, which were decreased significantly (P < 0.01) when compared with 2 mmol/L AA treatment group [80.6% and (44.3 +/- 4.0) micro m].

CONCLUSIONSAcrylamide has significant cytotoxicity and genotoxicity on HaCaT cells. AA-induced DNA damage may be related to the oxidative metabolite(s) of AA through CYP-450.

Acrylamide ; toxicity ; Cells, Cultured ; Cytochrome P-450 Enzyme Inhibitors ; DNA Damage ; Dose-Response Relationship, Drug ; Humans ; Keratinocytes ; drug effects ; enzymology

Acrylamide is a common chemical material, extensively used in industry and scientific experiments. Recently, it has been reported that starchy food cooked at high temperature can produce acrylamide. Acrylamide monomer has several toxic effects and the extensive concern for its toxicity has arisen with the finding of acrylamide formation in some processed foods. Researches have shown that acrylamide monomer can cause reproductive toxicity, including toxic effects on male reproductive behavior, male reproductive endocrine function and spermatogenesis. The mechanisms may include the effects of acrylamide on Leydig cells, the formation of motor protein/ chromosomal/DNA alkylation and damage by oxidative stress.
Acrylamide ; toxicity ; Animals ; Genitalia, Male ; drug effects ; physiology ; Male ; Sexual Behavior, Animal ; drug effects ; physiology ; Spermatogenesis ; drug effects

OBJECTIVETo explore effects of acrylamide on synaptic plasticity of rat neuron and its mechanisms.

METHODS24 Wistar rats were divided into control and test groups randomly, 12 rats in each group. The ratio of male and female in each group was 1:1. Acrylamide (30 mg/kg) was administered to rats by intraperitoneal injection in test group and normal saline (5 g/kg) was given to rats in control group. The neurobehavioral and pathologic changes of heart, liver, spleen, lung and kidney were observed. Changes of parameters in synapse were recorded by electron microscope. As an important target of synapse, change of Synapsin I was measured by immunohistochemical method.

RESULTSCompared with the control group (male: 1.00 ± 0.00; female: 1.00 ± 0.00), the gait score was increased significantly in ACR treated group (male: 2.50 ± 0.55, t = -7.24, P < 0.01; female: 3.17 ± 0.41, t = -12.19, P < 0.01). No obvious pathological changes of heart, liver, spleen, lung and kidney were found in all rats. Compared with the control group (male: (0.41 ± 0.09) µm; female: (0.40 ± 0.06) µm), the length of active zone of synapse was decreased significantly in ACR treated group (male: (0.15 ± 0.05) µm, t = 6.59, P < 0.05; female: (0.14 ± 0.07) µm, t = 7.26, P < 0.05). The width and postsynaptic density of synapse in ACR treated group had no significant difference with control group. The location of Synapsin I of control group and ACR treated group was both in gray matter of spinal dorsal horn. Compared with the control group (male: 195.40 ± 12.30; female: 195.19 ± 6.71), the concentration of Synapsin I was decreased significantly in ACR treated group (male: 60.90 ± 29.19, t = 10.40, P < 0.05; female: 67.56 ± 20.23, t = 15.65, P < 0.05).

CONCLUSIONNeuronal synaptic plasticity was found in damage of nervous system induced by acrylamide in rats, which might be associated with the expression of Synapsin I.

Acrylamide ; toxicity ; Animals ; Female ; Male ; Neuronal Plasticity ; drug effects ; Neurons ; drug effects ; Rats ; Rats, Wistar ; Synapses ; drug effects

The purpose of this study was to study the role of neurofilament (NF) mRNA and calpain in NF reduction of acrylamide (ACR) neuropathy. Male Wistar adult rats were injected i.p. every other day with ACR (20 mg/kg·bW or 40 mg/kg·bW) for 8 weeks. NF mRNA expression was detected using RT-PCR and the calpain concentration was determined using western blot analysis. The NF mRNA expression significantly decreased while the level of m-calpain and μ-calpain significantly increased in two ACR-treated rats groups regardless of the ACR dose. The light NF (NF-L) protein expression was significantly correlated with NF-L mRNA expression. Combined with previous data, the concentrations of three NF subunits were negatively correlated with the calpain levels. These findings suggest that NF-L mRNA and calpain mediated the reduction in NF of ACR neuropathy.
Acrylamide ; toxicity ; Animals ; Calpain ; metabolism ; Gene Expression Regulation ; drug effects ; Intermediate Filaments ; genetics ; Male ; Peripheral Nervous System Diseases ; chemically induced ; genetics ; metabolism ; RNA, Messenger ; genetics ; metabolism ; Rats

OBJECTIVETo explore the effects of acrylamide on the permeability of blood cerebrospinal fluid barrier (BCB) and tight junction protein ZO-1 of choroid plexus in rats and to provide a theoretical basis for explaining the mechanism of nerve injury induced by acrylamide.

METHODSThirty two male Sprague-Dawley rats were randomly divided into ACR and control groups. ACR group was exposed to 20 mg/kg ACR daily for 5 days a week by intraperitoneal injection (i.p.) for 4 weeks. Control group was exposed to normal saline. The neurobehavioral tests (including sensatory and motor functions) were performed every week. At the end of exposure, Evan blue (EB) and Sodium fluorescein (NaFI) content in rat CSF were detected for determining the BCB permeability, Real-time PCR was used to measure the expression levels of ZO-1 mRNA in the epithelium cells of choroid plexus, and laser scanning confocal microscope (LSCM) was utilized to observe the distribution of ZO-1 protein.

RESULTSNeurobehavioral tests showed that the tail-flick latencies of ACR group were 27.77% and 53.71% as long as control group in the 3rd week and 4th week, respectively (P < 0.05). The hind lamb splay distances of ACR group were 131.76% and 153.77% as long as control group in the 3rd week and 4th week, respectively (P < 0.05). Evan blue (EB) and Sodium fluorescein (NaFI) content of ACR group were significantly higher than those of control group (P < 0.05). In the 4th week, the expression level of ZO-1 mRNA in ACR group was 0.21 +/- 0.07, which was significantly lower than that (0.31 +/- 0.11) in control group (P < 0.05). In the 4th week, the ZO-1 protein expression level of choroid plexus in ACR group was significantly lower than that in control group (P < 0.05).

CONCLUSIONAcrylamide could increased the BCB permeability of rats, which may be involved in the central nervous injury induced by ACR.

Acrylamide ; toxicity ; Animals ; Blood-Brain Barrier ; drug effects ; Choroid Plexus ; metabolism ; Male ; Permeability ; drug effects ; Rats ; Rats, Sprague-Dawley ; Zonula Occludens-1 Protein ; metabolism

OBJECTIVETo evaluate the hazardous effects of fried potato chips upon the retina of two developmental stages of the albino rats aged 7 and 14 days from parturition.

METHODSPREGNANT RATS WERE ARRANGED INTO TWO GROUPS: control pregnant rats and consequently their delivered newborns until reaching 7 and 14 days old from parturition and fried potato chips group in which pregnant rats at the 6th day of gestation maintained on diet formed of fried potato chips supplied from the market mixed with standard diet at a concentration of 50% per each till 7 and 14 post-partum. Three fold integrated approaches were adopted, namely, histological, ultrastructural and proteomic analysis.

RESULTSHistological examination of the retina of the experimental offsprings revealed many histopathological changes, including massive degeneration, vacuolization and cell loss in the ganglion cell layer, as well as general reduction in retinal size. At the ultrastructural level, the retina of experimental offsprings exhibited number of deformities, including ill differentiated and degenerated nuclear layer, malformed and vacuolated pigment epithelium with vesiculated and fragmented rough endoplasmic reticulum, degenerated outer segment of photoreceptors, as well as swollen choriocapillaris and loss of neuronal cells. Proteomic analysis of retina of the two experimental developmental stages showed variations in the expressed proteins as a result of intoxication which illustrated the adverse toxic effects of fried potato chips upon the retina.

CONCLUSIONSIt can be concluded that the effect of fried potato chips on the development of retina in rats may be due to the presence of acrylamide or its metabolite.

Acrylamide ; toxicity ; Animals ; Animals, Newborn ; Cooking ; methods ; Diet ; methods ; Female ; Histocytochemistry ; Male ; Pigments, Biological ; Pregnancy ; Proteome ; analysis ; Rats ; Retina ; pathology ; Solanum tuberosum ; chemistry ; Ultrasonography

OBJECTIVETo investigate the mechanism of acrylamide (AA)-induced mutational spectra in the tk gene of mouse lymphoma cells.

METHODSL5178Y3.2.7c-tk(+/-) cells were treated with AA at different concentrations. Mutational spectra of tk locus were analyzed by the mouse lymphoma assay (microtiter procedure), and frequency of loss of heterozygosity (LOH) analysis with allele special PCR. Subsequently determined the DNA sequence of negative LOH's colonies induced by AA.

RESULTSThe LOH of mutants derived from AA induction was 78.8%, and showed a good dose-response relationship in large colonies. The occurrence of LOH of large colonies at lower doses (150 microg/ml and 300 microg/ml) were 25.0% and 33.3% respectively which were significantly different from those of control (66.7%), and at higher doses (600 microg/ml and 750 microg/ml) were 77.8% and 85.7%. By Sequence analysis showed that AA-induced point mutations were mainly base substitutions, and most of them were T:G-->G:T transversions.

CONCLUSIONFunctional tk allele gene loss is major mutational event in both spontaneous and induced tk mutants. And point mutations were base substitution.

Acrylamide ; toxicity ; Animals ; Cell Line, Tumor ; DNA Mutational Analysis ; Dose-Response Relationship, Drug ; Loss of Heterozygosity ; drug effects ; Lymphoma ; enzymology ; genetics ; Mice ; Point Mutation ; Thymidine Kinase ; genetics

OBJECTIVEThe content of acrylamide increases remarkably in fried, baked and heat-processed starchy foods. The present experiment was aimed at investigating the toxicity of acrylamide on the reproductive system in male rats.

METHODSThirty weaned 21-day-old SD male rats were randomly allotted into three groups of 10 each. Group I and Group II were fed on water solutions containing acrylamide 5 mg/kg/d and 10 mg/kg/d for eight consecutive weeks, while the third group on fresh water only as the control. The body weight, viscera weights and testicle and epididymis tissues were detected at the fourth and eighth week respectively. In the end of the experiment, the sperm reserve and morphology in the cauda of the epididymis were examined.

RESULTSThe growth of the rats treated with acrylamide was retarded (P < 0.05). The weights of the testis and epididymis and the sperm concentration in the cauda of the epididymis of Group II were decreased significantly (P < 0.05) after acrylamide administration, while no significant change was observed in the sperm concentration of Group I (P > 0.05). Furthermore, histopathological lesions were presented in the testes of the treated rats, and the number of Leydig cells around the apoptosis seminiferous tubules increased significantly (P < 0.05).

CONCLUSIONAcrylamide has toxic effects on seminiferous tubules and decreases the production of sperm in male rats.

Acrylamide ; toxicity ; Administration, Oral ; Animals ; Epididymis ; drug effects ; pathology ; Male ; Organ Size ; Random Allocation ; Rats ; Rats, Sprague-Dawley ; Sperm Count ; Sperm Motility ; Testis ; drug effects ; pathology