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PubMedDate not supplied

Protective role of Panax ginseng extract standardized with ginsenoside Rg3 against acrylamide-induced neurotoxicity in rats.

Acrylamide (ACR) is an industrial neurotoxic chemical that has been recently found in carbohydrate-rich foods cooked at high temperatures. ACR was designated as a probable human carcinogen by IARC (1994) and USEPA (1988). Panax ginseng extract has efficacies such as anticancer, antihypertension, antidiabetes and antinociception. The objective of the current study is to evaluate the protective effects of Panax ginseng extract against ACR-induced toxicity in rats. Sixty adult Sprague Dawley female rats were divided into six groups included a control group, a group treated orally with ACR (50 mg kg(-1) body weight; b.w.) for 11 days, a group treated orally with Panax ginseng extract (20 mg kg(-1) b.w.) for 11 days and groups treated orally with Panax ginseng for 11 days before, during or after 11 days of ACR treatment. The results indicated that treatment with ACR alone resulted in a significant increase in lipid peroxidation level and LDH activity in brain homogenate as well as in serum CK activity, whereas it caused a significant decrease in SOD activity and a small but statistically insignificant decrease in Na(+)K(+)-ATPase activity in brain homogenate. Serum serotonin, corticosterone, T3, T4, TSH, estradiol, progesterone and plasma adrenaline were significantly decreased in ACR-treated rats. Treatment with Panax ginseng before, during or after ACR treatment reduced or partially antagonized the effects induced by ACR towards the normal values of controls. It could be concluded that Panax ginseng extract exhibited a protective action against ACR toxicity and it is worth noting that treatment with Panax ginseng extract before or at the same time as ACR treatment was more effective than when administered after ACR treatment.

Acrylamide↗
PubMed2005

Effect of subchronic acrylamide exposure on the expression of neuronal and inducible nitric oxide synthase in rat brain.

Acrylamide (ACR) is a known industrial neurotoxic chemical. Evidence suggests that ACR neurotoxic effect is related to brain neurotransmission disturbances. Since nitric oxide (NO) acts as a neurotransmission modulator and is produced by nitric oxide synthase (NOS), the neuronal NOS (nNOS) and inducible NOS (iNOS) expression pattern were determined in rat cerebral cortex and striatum after subchronic exposure to ACR. Using immunocytochemistry, the neuronal count of nNOS or optical density of iNOS from sections at three coronal levels, bregma 1.0, -0.4, and -2.3 mm, were compared between ACR-treated and control rats. At all three levels, nNOS expressions were uniformly decreased in most of the neocortical subregions following the treatment of ACR. At bregma level 1.0 mm, total numbers of nNOS expressing neurons were significantly decreased to 58.7% and 64.7% of the control in the cortex and striatum of ACR-treated rats, respectively. However, at the bregma level -2.3 mm, ACR treatment did not produce a significant difference in the numbers of nNOS expressing neurons both in the cortex and striatum. Contrary to nNOS, iNOS expressions were consistently increased to approximately 32% in the neocortex and 25% in the striatum, following the subchronic ACR treatment. These data suggest that subchronic ACR exposure involves compensatory mechanism on nNOS and iNOS expression to maintain the homeostasis of NO at the rostral part of the neocortex and the striatum. However, in the caudal brain, increased iNOS expression did not suppress nNOS expression. Therefore, the present study is consistent with the hypothesis that ACR toxicity is mediated through the disturbance to the NO signaling pathway and exhibits a rostrocaudal difference through the differential expressions of nNOS and iNOS in the neocortex and the striatum.

Acrylamide↗
PubMed2007

Sustained release pellets based on poly(N-isopropyl acrylamide): matrix and in situ photopolymerization-coated systems.

The usefulness of poly(N-isopropyl acrylamide), PNIPA, for preparing sustained release matrix or photopolymerization-coated cellulosic pellets was evaluated. Theophylline pellets and granules were prepared using powdered cellulose (PC), poly(vinylpyrrolidone) (PVP), and PNIPA of Mw approximately 330 kDa, Mn approximately 93 kDa and low critical solubility temperature approximately 32 degrees C. The low consistency of wet mass, evaluated by torsion rheometry, due to hydrophilic character of PNIPA at room temperature, favored extrusion-spheronization. Theophylline (20%) pellets prepared with 15% PNIPA, 20% PVP and 45% PC, and granules obtained using 40% PNIPA and 40% PC showed an enhanced, although limited, ability to sustain the release. This effect was notably promoted after compression (which provides slowly eroding tablets) or coating of individualized pellets. A new coating technique consisting in forming the polymer film by photo-polymerization/cross-linking of NIPA monomers on pellets surface, using a photoinitiator and UV-irradiation at 366 nm, was developed. The composition of coating mixture and the time of irradiation were optimized using oscillatory rheometry. Coating did not significantly change the shape, size, or friability of the pellets but remarkably decreased the porosity and sustained drug release for several hours. In situ formation and cross-linking of PNIPA on the pellet appears as a feasible way for controlling drug release.

Acrylamides↗
PubMed2005

pH/temperature - sensitive imprinted ionic poly(N-tert-butylacrylamide-co-acrylamide/maleic acid) hydrogels for bovine serum albumin.

In this study, we have prepared pH/temperature-sensitive imprinted ionic poly(N-tert-butylacrylamide-co-acrylamide/maleic acid) [P(TBA-co-AAm/MA)] hydrogels for bovine serum albumin (BSA) by using molecular imprinting method. BSA adsorption from aqueous BSA solutions was investigated with two types of hydrogel systems prepared by non-imprinted and imprinted methods. Hydrogels imprinted with BSA showed higher adsorption capacity and specificity for BSA than hydrogels prepared by the usual procedure. At all studied conditions, the highest BSA adsorption was observed in the hydrogel imprinted with 8.63 wt.-% BSA. In addition, the imprinted hydrogels exhibited both for good selectivity BSA and high adsorption rate depending on the number of BSA-sized cavities. Adsorption studies showed that other stimuli, such as pH, temperature and initial BSA concentration also influenced the BSA adsorption capacity of both non-imprinted and imprinted hydrogels.

Acrylamides↗
PubMed2005

Preparation and characterisation of thermoresponsive poly[(N-isopropylacrylamide-co-acrylamide-co-(hydroxyethyl acrylate)] microspheres as a matrix for the pulsed release of drugs.

Despite the large number of publications and patents concerning pH/thermoresponsive polymers, few data are available concerning the preparation of thermoresponsive cross-linked microspheres from preformed polymers. Therefore, N-isopropylacrylamide-co-acrylamide-co-(2-hydroxyethyl acrylate) copolymers were obtained as a new thermoresponsive material with a lower critical solution temperature (LCST) around 36 degrees C, in phosphate buffer at pH 7.4, and with a cross-linkable OH group in their structure. The LCST value was determined both by UV spectroscopy and microcalorimetric analysis. These copolymers were solubilised in acidified aqueous solution below their LCST, dispersed in mineral oil, and transformed into stable microspheres by cross-linking with glutaraldehyde. The thermoresponsive microspheres were characterised by optical and scanning electron microscopy, degree of swelling, and water retention. The pore dimensions of the microspheres and the retention volumes of some drugs and typical compounds were evaluated at different temperatures by liquid chromatography. Indomethacin, as a model drug, was included in the microspheres by the solvent evaporation method. Finally, the influence of temperature and of temperature cycling on drug release was investigated.

Acrylamides↗
PubMed1989

Slow recovery of central axons in acrylamide neuropathy.

To study the differential vulnerability of central versus peripheral axons, we observed serial changes in conduction over comparable segments of central and peripheral axons of the primary sensory neuron in 17 rats with acrylamide neuropathy using somatosensory evoked potentials. Central conduction abnormalities persisted even after peripheral conduction and clinical abnormalities had recovered. Morphometric studies showed prompt restoration of the largest-diameter fibers in the peripheral nerve after clinical recovery but persistent or even more severe loss of large- and medium-sized fibers in the cervical gracile tract. This finding suggests that recovery from central-peripheral distal axonopathy begins in the largest peripheral axons, perhaps even at the expense of central axons, and that clinical recovery can occur at a time when central conduction remains abnormal. The selective central axonopathy found in certain chronic degenerative disorders may be a consequence of this slow central recovery process associated with chronic or intermittent metabolic derangements.

Acrylamides↗
PubMed2002

Protective effect of acorus calamus against acrylamide induced neurotoxicity.

Exposure of rats to acrylamide (ACR) caused hind limb paralysis in 58% of the animals on day 10 and decreased behavioural parameters, namely distance travelled, ambulatory time, stereotypic time and basal stereotypic movements compared with the control group. These rats also had a decrease in the reduced glutathione (GSH) content and glutathione-S-transferase (GST) activity in the corpus striatum and an increase in striatal dopamine receptors, as evident by an increase in the binding of 3H-spiperone to striatal membranes. Treatment with the ethanol:water (1:1) extract of the rhizomes of Acorus calamus (AC-002) increased the GSH content and GST activity in the corpus striatum while insignificant changes were observed in other parameters. Rats treated with ACR and AC-002 in combination had a lower incidence of paralysis (18%) compared with those treated with ACR alone on day 10 of the experiment. The rats also showed a partial recovery in other behavioural parameters. The levels of GSH content and GST activity increased in the corpus striatum, while the dopamine receptors decreased compared with the ACR treated rats. The results suggest that the neurobehavioural changes produced by ACR may be prevented following treatment with Acorus calamus rhizomes.

Acorus↗
PubMed1999

Simultaneous analysis of hemoglobin adducts of acrylamide and glycidamide by gas chromatography-mass spectrometry.

Acrylamide (AA) is a carcinogen in experimental animals. Glycidamide (GA), formed by metabolic epoxidation of AA, is believed to be responsible for the carcinogenicity of AA. Occupational exposure to AA has been assessed earlier by measurement of its adducts with N-terminal valine in hemoglobin. A background of AA adducts [N-(2-carbamoylethyl)valine (AAVal), about 30 pmol/g globin] was found in individuals without known exposure to the compound. The method previously available for adducts of GA only allowed analysis of samples from highly exposed individuals and showed similar levels of AAVal and adducts of GA [N-(2-hydroxy-2-carbamoylethyl)valine (GAVal)]. We have developed a sensitive method for simultaneous quantification of adducts of GA and AA, which is suitable down to low exposure levels. The method is based on the so-called modified Edman method, where globin is reacted with pentafluorophenyl isothiocyanate under neutral conditions. The valine adducts are then extracted in the form of pentafluorophenylthiohydantoin (PFPTH) derivatives. The analytical procedure included reaction of the PFPTH derivatives with acetic anhydride in order to protect the hydroxyl group of GAVal. The PFPTH derivatives of AAVal and GAVal were analyzed by gas chromatography/tandem mass spectrometry. ((2)H(3))AAVal-PFPTH was used as the internal standard. The method was applied to samples from 11 workers at an AA production plant, 1 nonexposed nonsmoker, and a few participants of a smoking cessation program. AAVal levels were in the range 27-1854 pmol/g globin. Recorded levels of GAVal were 3-12% of those of AAVal, suggesting that previous measurements of GAVal overestimate GAVal at low levels of exposure to AA.

Acrylamide↗
PubMed2005

Acrylamide in food: the discovery and its implications: a historical perspective.

The unexpected finding that humans are regularly exposed to relatively high doses of acrylamide (AA) through normal consumption of cooked food was a result of systematic research and relevant developments in methodology over decades, as well as a chain of certain coincidences. The present paper describes the scientific approach, investigations and events leading to the discovery of the formation of AA during cooking of foods. In addition, related issues concerning assessment, communication and management of cancer risks and associated ethical questions raised by the finding of the presence of AA in foods will be discussed.

Acrylamide↗
PubMed2005

Mechanisms of acrylamide formation: Maillard-induced transformation of asparagine.

The formation of acrylamide (AA) from L-asparagine was studied in Maillard model systems under pyrolysis conditions. While the early Maillard intermediate N-glucosylasparagine generated approximately 2.4 mmol/mol AA, the Amadori compound was a less efficient precursor (0.1 mmol/mol). Reaction with alpha-dicarbonyls resulted in relatively low AA amounts (0.2-0.5 mmol/mol), suggesting that the Strecker aldehyde pathway is of limited relevance. Similarly, the Strecker alcohol 3-hydroxypropanamide generated low amounts of AA (0.2 mmol/mol). On the other hand, hydroxyacetone afforded more than 4 mmol/mol AA, indicating that alpha-hydroxycarbonyls are more efficient than alpha-dicarbonyls in transforming asparagine into AA. The experimental results are consistent with the reaction mechanism proposed, i.e. (i) Strecker-type degradation of the Schiff base leading to azomethine ylides, followed by (ii) beta-elimination of the decarboxylated Amadori compound to release AA. The functional group in beta-position on both sides of the nitrogen atom is crucial. Rearrangement of the azomethine ylide to the decarboxylated Amadori compound is the key step, which is favored if the carbonyl moiety contains a hydroxyl group in beta-position to the N-atom. The beta-elimination step in the amino acid moiety was demonstrated by reacting under pyrolysis conditions decarboxylated model Amadori compounds obtained by synthesis.

Acetone↗
PubMed2005

New aspects on the formation and analysis of acrylamide.

The effectiveness of different compounds in the generation of acrylamide (AA) from asparagine, was determined by reacting asparagine with mono-, di- and polysaccharides, as well as four different oxo-compounds known to be involved in carbohydrate metabolism/degradation. Quantitation of AA formed either under aqueous conditions or in low water model systems revealed glucose and 2-oxopropionic acid as the most effective compounds in AA generation, when reacted in model systems with a low water content (about 1 mol-% yield). Interestingly, heating of asparagine in the presence of 2-oxopropionic acid generated quite high amounts of 3-aminopropionamide (3-APA), which itself effectively generated AA upon heating in aqueous solution, as well as in low water systems. Because this is the first report on amounts of 3-APA generated by Maillard-type reactions, the general role of 3-APA as key intermediate in AA formation is discussed in detail. In addition, first results on the development and application of an HPLC/fluorescence method for AA quantitation are presented.

Acrylamide↗
PubMed2005

Acrylamide and glycidamide: approach towards risk assessment based on biomarker guided dosimetry of genotoxic/mutagenic effects in human blood.

Acrylamide (AA) is a carcinogen as demonstrated in animal experiments, but the relevance for the human situation is still unclear. AA and its metabolite glycidamide (GA) react with nucleophilic regions in biomolecules. However, whereas AA and GA react with proteins, DNA adducts are exclusively formed by GA under conditions simulating in vivo situations. For risk assessment it is of particular interest to elucidate whether AA or GA within the plasma concentration range resulting from food intake are "quenched" by preferential reaction with non-critical blood constituents or whether DNA in lymphocytes is damaged concomitantly under such conditions. To address this question dose- and time-dependent induction of hemoglobin (Hb) adducts as well as genotoxic and mutagenic effects by AA or GA were studied in human blood as a model system.

Acrylamide↗
PubMed1987

In vitro cytotoxicity of heavy metals, acrylamide, and organotin salts to neural cells and fibroblasts.

The cytotoxicity of neurotoxic agents was determined for a series of brain-derived cell types and compared with their toxic effects on BALB/c 3T3 fibroblasts, using the neutral red assay. Ranking of toxicants according to their potencies was the same for all cells tested and was in the order of methylmercury greater than cadmium greater than mercury greater than zinc greater than acrylamide. For a series of di- and triorganotins the ranking order was dibutyl greater than diphenyl greater than dibenzyl greater than dipropyl greater than diethyl greater than dimethyltin and triphenyl greater than tribenzyl greater than trimethyltin, respectively. The test was sensitive enough to detect structure activity relationships between the degree of toxicity and the hydrophobic characteristics of the agents tested.

Acrylamides↗
PubMed1988

Effects of N,N'-methylene-bis-acrylamide (MBA) on mouse germ cells--sperm count and morphology, and testicular pathology.

The sperm count and morphology, and testicular histopathology were studied in mice over a period of 75 days following a single oral administration of 50, 100, and 200 mg/kg N.N'-methylene-bis-acrylamide (MBA). With a 50 and 100 mg/kg dose, the sperm abnormality reached a maximum at 30 days, whereas the sperm count reached a minimum at 35 days. The abnormality and decrease in sperm count were both dose dependent. Following the administration of 200 mg/kg MBA, the appearance of abnormal sperm showed a diphase pattern, i.e., first at 7-15 days without any reduction of the sperm count and second at 30 days after treatment. Testicular histopathological changes showed that resting spermatocytes, succeeding leptotene and zygotene spermatocytes were either absent or reduced 1-3 days after treatment with 200 mg/kg MBA. These early histopathological changes seemed to precede both the increase in abnormal sperm and the decrease in sperm count observed 30-35 days post-treatment, and also suggested that resting spermatocytes were most sensitive to MBA exposure among various spermatogenic cells.

Acrylamides↗
PubMed1982

Anemia and porphyria caused by N,N'-methylene-bis-acrylamide (MBA) in mice and rats.

The effects of N,N'-methylene-bis-acrylamide (MBA), a cross-linking agent, on blood and bone marrow after repeated oral doses, were studied in mice and rats. Body weight, three major elements of the blood - erythrocytes, leucocytes and platelets -, reticulocytes and bone marrow cells, were all reduced in either or both animals, especially in mice. Phenobarbital (PB) treatment did not greatly modify the effects of MBA in mice. An increase in free erythrocyte porphyrins and a decrease in ALA-D activity were observed in both animals. Urinary porphyrins were elevated in rats after MBA-dosing. PB-treatment did not significantly affect the elevation of porphyrins. After cessation of the MBA-dosing, all these changes were inclined to be restored to normal levels. Amounts of liver total porphyrins and microsomal P-450, and red cell fragility were within normal ranges in mice.

Acrylamides↗
PubMed1979

Sequence of motor nerve terminal involvement in acrylamide neuropathy.

Acrylamide neuropathy is characterized by distal multifocal axonal degeneration. In this condition long and large myelinated fibers are affected more than sort and thin fibers. The purpose of the present study was to investigate the sequence of nerve terminal involvement. The study was limited to axons that belonged to one type of neuron, of approximately equal diameter but differing in length. Axon terminals from alpha motor neurons were investigated in five muscles from rats. The results show that the initial motor nerve terminal degeneration is widespread and not restricted to terminals of the longest axons with the largest volumes. It is suggested that the variation in degree of involvement of the motor nerve terminals is determined both by differences between endplates and the regenerative capacity of neurons.

Acrylamides↗
PubMed1982

Selective loss of Purkinje cells from the rat cerebellum caused by acrylamide and the responses of beta-glucuronidase and beta-galactosidase.

Acrylamide (30 mg/kg) given daily to rats five times each week for 3 weeks leads to progressive loss of Purkinje cells. The necrotic cells begin to be visible from the third day and their numbers reach a peak at the time when the dosing ceases at 18 days. They are less frequent thereafter, but are still visible almost 3 weeks later in small numbers. The density of Purkinje cells per millimeter falls to about 70% of normal at the 7th day, and a similar degree of reduction of the neuronal marker enzyme, beta-galactosidase, is found over the same time scale. By contrast, while there is a brisk macrophage/microglial response in the molecular layer to the loss of the Purkinje cell dendrites, the increase in beta-glucuronidase activity is relatively minor and is not significantly different from normal until after the 21st day. These responses are discussed in the context of the use of lysosomal enzyme activities in the assay of certain neurotoxic lesions.

Acrylamides↗