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PubMed2006

Impact of extraction conditions on the content of acrylamide in model systems and food.

It has recently been suggested that the analytical methods that have been developed to date for the determination of acrylamide (AA) may underestimate the concentration of AA in certain foods, because significantly higher results were obtained upon extraction of the food matrix under alkaline conditions. The present study employs food (potato, rye) and chemical model systems to better understand the tentative release of AA under high pH extraction conditions. The experimental design is based on the generation of AA in an environment containing an AA-isotopomer, and by comparing the ratio of AA, respectively the AA-isotopomer, after extraction at pHs 7 and 12. The results show that the additional AA released is not due to improved extractability of AA from the food matrix, and should therefore be regarded as an extraction artefact. Strongly alkaline conditions seem to induce net formation of AA from water-soluble precursors formed during thermolysis.

Acrylamide↗
PubMed2006

Determination of acrylamide in coffee and coffee products by GC-MS using an improved SPE clean-up.

An improved gas chromatography-mass spectrometry (GC-MS) method to determine acrylamide (AA) in coffee and coffee products was developed. The method was based on two main purification steps: the first with ethanol and Carrez solutions in order to precipitate polysaccharides and proteins, respectively; and the second with a layered solid-phase extraction (SPE) column which proved to be efficient in the elimination of the main chromatographic interferences. The method is applicable to a wide range of coffee products. Twenty-six samples of different coffee products were analysed. The levels of AA were in the range 11.4-36.2 microg l-1 for 'espresso coffee' and 200.8-229.4 microg l-1 for coffee blends with cereals. The results indicate that the presence of cereals significantly increased the levels of AA.

Acrylamide↗
PubMed2000

1-Aminobenzotriazole inhibits acrylamide-induced dominant lethal effects in spermatids of male mice.

Acrylamide (AA) is a germ cell mutagen and induces clastogenic effects predominantly in spermatids of mice. The mechanism of AA clastogenicity has been a matter of dispute. Since the reactivity of AA with DNA is low but is high with proteins containing SH groups, it was suggested that protamine alkylation could be the mechansim of clastogenicity by AA in spermatids. This was substantiated by the observation that the time course of protamine alkylation and dominant lethal effects in spermatids of mice induced by AA was strictly parallel. Another suggestion was that AA may be metabolized by cytochrome P-450 to the epoxide glycidamide (GA), which is then the ultimate DNA-reactive clastogen. This suggestion was based on the similarity of the stage specificity pattern for dominant lethality and heritable translocation induction by AA and GA. To test this latter assumption, 1-aminobenzotriazole (ABT), an inhibitor of P-450 metabolism, was used in the present experiments. Male mice were pretreated with ABT (3x50 mg/kg) on three consecutive days followed by AA treatment (125 mg/kg) on day 4. Parallel groups of animals were treated with AA (125 mg/kg), ABT (3x50 mg/kg) or with the solvent double-distilled water. The experiment was repeated once with slightly varied mating parameters. The results of both experiments showed that ABT inhibited or significantly reduced the AA-induced dominant lethal effects. Thus, the present data support the hypothesis that the AA metabolite GA is the ultimate clastogen in mouse spermatids.

Acrylamide↗
PubMed2001

Chromosomal composition of micronuclei in mouse NIH 3T3 cells treated with acrylamide, extract of Tripterygium hypoglaucum (level) hutch, mitomycin C and colchicine, detected by multicolor FISH with centromeric and telomeric DNA probes.

The chromosomal composition of micronuclei (MN) induced by the model mutagens mitomycin (MMC) and colchicine (COL) as well as by acrylamide (AA) and the traditional Chinese medicine Tripterygium hypoglaucum (level) hutch (THH) in NIH 3T3 cells was analyzed by multicolor fluorescence in situ hybridization (FISH) using DNA probes for the centromere repeated minor satellite DNA and the telomeric hexamer repeat (TTAGGG). The majority of MN (78.6%) from treatment with MMC (0.1 microg/ml) did not show centromeric signals, reflecting the clastogenic action of MMC. Following treatment with COL (0.1 microg/ml), 74.5% of the MN showed centromeric signals and several telomeric signals, indicating that MN induced by this well-known aneugen were mainly composed of whole chromosomes. After treatment with AA (100, 200 and 400 microg/ml) both MN containing whole chromosomes and MN containing acentric fragments were found to increase in a dose-dependent manner, demonstrating that AA is not only a clastogen but also an aneugen. THH induced a high frequency of MN harboring whole chromosomes at all concentrations tested (5, 10 and 20 microl/ml) and produced a dose-dependent increase in fragment-containing MN, indicating that THH has both aneugenic and clastogenic potential.

3T3 Cells↗
PubMed1975

Purification of S1 muclease from Takadiastase by affinity chromatography on single-stranded DNA-acrylamide columns.

When S1 nuclease from Takadiastase was partially purified according to previously reported methods, it showed a 10 to 15 fold increase in specificactivity. Although such preparations were highly active on single-stranded DNA, they had traces of activity on native DNA and were contaminated by T1-RNase. The S1 enzyme was further purified by a single step of affinity chromatography on single-stranded DNA-acrylamide column to a final purification of 275-fold. This preparation was free of T1-RNase and had an absolute specificity for single-stranded DNA.

Acrylamides↗
PubMed2003

Acrylamide: a comparison of metabolism and hemoglobin adducts in rodents following dermal, intraperitoneal, oral, or inhalation exposure.

Acrylamide (AM), which is used to manufacture polymers, is carcinogenic and a reproductive and neurological toxicant. The objective of this study was to compare the metabolism of AM administered orally (po), dermally, intraperitoneally (ip), or by inhalation, and to measure the hemoglobin adducts produced. Rats and mice were exposed to 2.9 ppm [1,2,3-13C] and [2,3-14C]AM for 6 h. [2,3-14C]AM (162 mg/kg) or [1,2,3-13C]AM (13 8 mg/kg) in water was administered dermally to rats for 24 h, and [1,2,3-13C]AM was administered ip (47 mg/kg). Urine and feces were collected for 24 h. Urine was the major elimination route in rats (ip, 62% and po, 53% of the dose; dermal, 44% of the absorbed dose; inhalation, 31% of the recovered radioactivity) and mice (inhalation, 27% of the recovered radioactivity). Signals in the 13C-NMR spectra of urine were assigned to previously identified metabolites derived from AM glutathione conjugation (AM-GSH) and conversion to glycidamide (GA). AM-GSH was a major metabolic route in rats accounting for 69% (ip), 71% (po), 52% (dermal), and 64% (inhalation). In mice, AM-GSH accounted for only 27% (inhalation) of the total urinary metabolites. The remaining urinary metabolites were derived from GA. Valine hemoglobin adducts of AM and GA were characterized using liquid chromatography-mass spectrometry. The ratio of AM to GA adducts paralleled the flux through pathways based on urinary metabolites. This study demonstrates marked species differences in the metabolism and internal dose (Hb-adducts) of AM following inhalation exposure and marked differences in uptake comparing dermal with po and ip administration.

Acrylamide↗
PubMed2004

Metabolism and hemoglobin adduct formation of acrylamide in humans.

Acrylamide (AM), used in the manufacture of polyacrylamide and grouting agents, is produced during the cooking of foods. Workplace exposure to AM can occur through the dermal and inhalation routes. The objectives of this study were to evaluate the metabolism of AM in humans following oral administration, to compare hemoglobin adduct formation on oral and dermal administration, and to measure hormone levels. The health of the people exposed under controlled conditions was continually monitored. Prior to conducting exposures in humans, a low-dose study was conducted in rats administered 3 mg/kg (1,2,3-13C3) AM by gavage. The study protocol was reviewed and approved by Institute Review Boards both at RTI, which performed the sample analysis, and the clinical research center conducting the study. (1,2,3-13C3) AM was administered in an aqueous solution orally (single dose of 0.5, 1.0, or 3.0 mg/kg) or dermally (three daily doses of 3.0 mg/kg) to sterile male volunteers. Urine samples (3 mg/kg oral dose) were analyzed for AM metabolites using 13C NMR spectroscopy. Approximately 86% of the urinary metabolites were derived from GSH conjugation and excreted as N-acetyl-S-(3-amino-3-oxopropyl)cysteine and its S-oxide. Glycidamide, glyceramide, and low levels of N-acetyl-S-(3-amino-2-hydroxy-3-oxopropyl)cysteine were detected in urine. On oral administration, a linear dose response was observed for N-(2-carbamoylethyl)valine (AAVal) and N-(2-carbamoyl-2-hydroxyethyl)valine (GAVal) in hemoglobin. Dermal administration resulted in lower levels of AAVal and GAVal. This study indicated that humans metabolize AM via glycidamide to a lesser extent than rodents, and dermal uptake was approximately 6.6% of that observed with oral uptake.

Acrylamide↗
PubMed2005

Role of CYP2E1 in the epoxidation of acrylamide to glycidamide and formation of DNA and hemoglobin adducts.

Acrylamide (AA) is an animal carcinogen, neurotoxin, and reproductive toxin. AA is formed in baked and fried carbohydrate-rich foods. Metabolism of AA occurs via epoxidation to glycidamide (GA) or direct conjugation with glutathione. Using CYP2E1-null mice, recent studies in this laboratory demonstrated that induction of somatic and germ cell mutagenicity in AA-treated mice is dependent on CYP2E1. We hypothesized that AA metabolism to GA is a prerequisite for the induction of AA-induced mutagenicity. Current studies were undertaken to assess the role of CYP2E1 in the epoxidation of AA to GA and the formation of DNA and hemoglobin (HGB) adducts. AA was administered to CYP2E1-null or wild-type mice at 50 mg/kg ip. Mice were euthanized 6 h later and blood and tissues were collected. Using LC-ES/MS/MS, AA, GA, and DNA- and HGB-adducts were measured. While the plasma levels of AA and GA were 115 +/- 14.0 and 1.7 +/- 0.31 microM in CYP2E1-null mice, they were 0.84 +/- 0.80 and 33.0 +/- 6.3 microM in the plasma of AA-treated wild-type mice. Administration of AA to wild-type mice caused a large increase in N7-GA-Gua and N3-GA-Ade adducts in the liver, lung, and testes. While traces of N7-GA-Gua adducts were measured in the tissues of AA-treated CYP2E1-null mice, these levels were 52- to 66-fold lower than in wild-type mice. Significant elevation of both AA- and GA-HGB adducts was detected in AA-treated wild-type mice. In AA-treated CYP2E1-null mice, levels of AA-HGB adducts were roughly twice as high as those in wild-type mice. In conclusion, current work demonstrated that CYP2E1 is the primary enzyme responsible for the epoxidation of AA to GA, which leads to the formation of GA-DNA and HGB adducts.

Acrylamide↗
PubMed2005

Acrylamide inhibits dopamine uptake in rat striatal synaptic vesicles.

Evidence suggests that acrylamide (ACR) neurotoxicity is mediated by decreased presynaptic neurotransmitter release. Defective release might involve disruption of neurotransmitter storage, and therefore, we determined the effects of in vivo and in vitro ACR exposure on 3H-dopamine (DA) transport into rat striatal synaptic vesicles. Results showed that vesicular DA uptake was decreased significantly in rats intoxicated at either 50 mg/kg/day x 5 days or 21 mg/kg/day x 21 days. ACR intoxication also was accompanied by a reduction in KCl-evoked synaptosomal DA release, although consistent changes in presynaptic membrane transport were not observed. Silver stain and immunoblot analyses suggested that reduced vesicular uptake was not due to active nerve terminal degeneration or to a reduction in the synaptic vesicle content of isolated striatal synaptosomes. Nor did the in vivo presynaptic effects of ACR involve changes in synaptosomal glutathione concentrations. In vitro exposure of striatal vesicles showed that both ACR and two sulfhydryl reagents, N-ethylmaleimide (NEM) and iodoacetic acid (IAA), produced concentration-dependent decreases in 3H-DA uptake. Although ACR was significantly less potent than either NEM or IAA, all three chemicals caused comparable maximal inhibitions of vesicular uptake. Kinetic analysis of DA uptake showed that in vitro exposure to either ACR or NEM decreased V(max) and increased K(m). Determination of radiolabel efflux from 3H-DA-loaded vesicles indicated that in vitro ACR did not affect neurotransmitter retention. These data suggest that ACR impaired neurotransmitter uptake into striatal synaptic vesicles, possibly by interacting with sulfhydryl groups on functionally relevant proteins. The resulting disruption of neurotransmitter storage might mediate defective presynaptic release.

Acrylamide↗
PubMed2006

Kinetics of elimination of urinary metabolites of acrylamide in humans.

Acrylamide (AM), used in the manufacture of polyacrylamide and grouting agents, is produced during the cooking of foods. Workplace exposure to AM can occur through the dermal and inhalation routes. The objective of this study was to define the kinetics of elimination of AM and its metabolites following oral and dermal administration. This is the second part of a study in which metabolites and hemoglobin adducts of AM were determined in people (Fennell et al., 2005, Toxicol. Sci. 85, 447-459). (1,2,3-(13)C(3))AM was administered in an aqueous solution orally (single dose of 0.5, 1.0, or 3.0 mg/kg) or dermally (three daily doses of 3.0 mg/kg) to sterile male volunteers. Urine samples were collected at 0-2, 2-4, 4-8, 8-16, and 16-24 h following administration orally, or at 0-2, 2-4, 4-8, 8-16, and 16-24 h following each of three daily dermal doses. (13)C(3)-AM and its metabolites in urine, (13)C(3)-glycidamide, (13)C(3)-N-acetyl-S-(3-amino-3-oxopropyl)cysteine and its S-oxide, and (13)C(3)-N-acetyl-S-(3-amino-2-hydroxy-3-oxopropyl)cysteine, were quantitated using liquid chromatography-tandem mass spectrometry. The recovered urinary metabolites accounted for 45.6, 49.9, and 39.9% of a 0.5, 1.0, and 3.0 mg/kg oral dose (0-24 h), respectively, and for 4.5% of the dose after 3 mg/kg was administered daily for 3 days dermally (0-4 days). These results indicate that after oral administration AM is rapidly absorbed and eliminated. The half-life estimated for elimination of AM in urine was 3.1-3.5 h. After dermal administration, AM uptake is slow. This study indicated that skin provides a barrier that slows the absorption of AM, and results in limited systemic availability following dermal exposure to AM.

Acetylcysteine↗
PubMed2006

Cytogenetic damage induced by acrylamide and glycidamide in mammalian cells: correlation with specific glycidamide-DNA adducts.

Acrylamide (AA) is a suspected human carcinogen generated in carbohydrate-rich foodstuffs upon heating. Glycidamide (GA), formed via epoxidation, presumably mediated by cytochrome P450 2E1, is thought to be the active metabolite playing a central role in AA genotoxicity. In this work we investigated DNA damage induced by AA and GA in mammalian cells, using V79 Chinese hamster cells. For this purpose, we evaluated two cytogenetic end points, chromosomal aberrations (CAs) and sister chromatid exchanges (SCEs), as well as the levels of specific GA-DNA adducts, namely, N7-(2-carbamoyl-2-hydroxyethyl)guanine (N7-GA-Gua) and N3-(2-carbamoyl-2-hydroxyethyl)adenine (N3-GA-Ade) using high-performance liquid chromatography coupled with tandem mass spectrometry. GA was more cytotoxic and clastogenic than AA. Both AA and GA induced CAs (breaks and gaps) and decreased the mitotic index. GA induced SCEs in a dose-responsive manner; with AA, SCEs were increased at only the highest dose tested (2mM). A linear dose-response relationship was observed between the GA concentration and the levels of N7-GA-Gua. This adduct was detected for concentrations as low as 1 microM GA. N3-GA-Ade was also detected, but only at very high GA concentrations (>or= 250 microM). There was a very strong correlation between the levels of N7-GA-Gua in the GA- and AA-treated cells and the extent of SCE induction. Such correlation was not apparent for CAs. These data suggest that the induction of SCEs by AA is associated with the metabolism of AA to GA and subsequent formation of depurinating DNA adducts; however, other mechanisms must be involved in the induction of CAs.

Acrylamide↗
PubMed1983

Altered sensory ganglia in acrylamide neuropathy. Quantitative evidence of neuronal reorganization.

To learn more about the nerve cell body in neurotoxin-induced degeneration of axons, Sprague-Dawley rats were intoxicated with 50 mg/kg/day of the prototype neurotoxin acrylamide monomer. The lumbar dorsal root ganglia were studied in those rats with progressive disease (controls were not intoxicated). Qualitative changes in cytological organization included nuclear eccentricity, reduction in the size of Nissl bodies or displacement to a peripheral mantle, and marked enlargement of mitochondria. Quantitatively, there were statistically significant increases in these alterations, occurring early during disease and progressing over time. A stereological analysis showed a significant increase in the volume density of mitochondria, a significant decrease in Nissl bodies, but no change in the Golgi apparatus. The data suggest that cell body alterations may represent a progressive, orderly reorganization, supporting the concept that the cell body functions in determining the fate of intoxicated neurons.

Acrylamides↗
PubMed1988

Neurofilament antigens in acrylamide neuropathy.

After repeated exposure, acrylamide (AC) produces degeneration of distal axons. Because neurons whose axons have been injured (e.g. by axotomy) show alterations in their structural and chemical properties, the present study was designed to differentiate the direct effects of AC intoxication from neuronal responses secondary to axonal injury caused by AC. Rats were given AC as either a single high dose (75 mg/kg), or as daily intraperitoneal injections (30 mg/kg, six days per week for four weeks). Dorsal root ganglia of the fifth lumbar level, L5, were examined using a variety of monoclonal antibodies directed against nonphosphorylated (2-135) and phosphorylated (03-44, 06-17, 07-05) epitopes of 145 and 200 kilodalton neurofilament proteins. In control rats, antibody 2-135 stained axons and neuronal cell bodies; antibodies against phosphorylated epitopes of neurofilaments stained only axons distal to the glomerulus. Following chronic AC intoxication, all three antibodies directed against phosphorylated epitopes of neurofilaments (particularly 07-05) demonstrated intense immunoreactivity in 20-30% of neuronal cell bodies. In addition, the glomerular region of these axons was stained. Electron microscopy revealed many chromatolytic cells containing few neurofilaments. In contrast, a single high dose of AC produced no abnormal staining of neuronal cell bodies at a time when slow axonal transport was impaired. Our findings are compared to those observed following axotomy and to those occurring in aluminum-intoxicated rabbits, two experimental disorders in which altered distributions of phosphorylated filaments have been documented.

Acrylamides↗
PubMed2007

Mortality patterns among workers exposed to acrylamide: updated follow up.

OBJECTIVE: The objective of this study was to update the mortality experience of a cohort of workers with and without potential exposure to acrylamide (AMD) at three U.S. plants (n = 8508) and one plant in The Netherlands (n = 344). METHODS: We computed standardized mortality ratios (SMRs) using national and local rates and modeled internal cohort rates to assess site-specific cancer risks by demographic and work history factors and several exposure indicators for AMD. RESULTS: For the 1925-2002 study period, we observed both deficit and excess overall mortality risks among the U.S. cohort for cancer sites implicated in experimental animal studies: brain and other central nervous system (SMR = 0.67, confidence interval [CI] = 0.40-1.05), thyroid gland (SMR = 1.38, CI = 0.28-4.02), testis and other male genital organs (SMR = 0.64, CI = 0.08-2.30); and for sites selected in earlier exploratory analyses of this cohort: respiratory system cancer (RSC) (SMR = 1.17, CI = 1.06-1.27), esophagus (SMR = 1.20, CI = 0.86-1.63), rectum (SMR = 1.25, CI = 0.84-1.78), pancreas (SMR = 0.94, CI = 0.70-1.22), and kidney (SMR = 1.01, CI = 0.66-1.46). Except for RSC, attributed earlier to muriatic acid exposure, none of the mortality excesses was statistically significant. In the Dutch cohort, we observed deficits in deaths for all sites of a priori interest. An updated analysis of our previous exploratory findings for pancreatic cancer in the U.S. cohort revealed much less evidence of a possible exposure-response relationship with AMD. CONCLUSION: AMD exposure at the levels present in our study sites was not associated with elevated cancer mortality risks.

Acrylamide↗
PubMedDate not supplied

The pathokinetics of acrylamide intoxication: a reassessment of the problem.

Acrylamide was given intraperitoneally to rats (30 mg/kg/day, five times/week) for 3 weeks, and the nervous and muscle tissues were examined by conventional methods over 5 weeks. Three striking cellular changes were observed. 1 Scattered degeneration of many Purkinje cells from 5 days onwards. 2 Widespread swelling and argyrophilia of nerve terminals from 10 days in both PNS and CNS. Motor and sensory endings were equally affected in all muscles examined. Synaptic and preterminal swelling also occurred in spinal cord, brain stem, and in certain cerebellar terminals. Degeneration occasionally followed this change, particularly in sensory nerve fibres, but not necessarily. 3 Chromatolysis in spinal ganglion cells and occasionally in anterior horn cells from 7 days onwards before the onset of axonal degeneration. This unique sequence of events is discussed in the light of the metabolic and other changes described by earlier authors.

Acrylamides↗
PubMedDate not supplied

Acrylamide-induced remodelling of perikarya in rat superior cervical ganglia.

To extend investigations on how acrylamide affects neuronal perikarya, we studied post-ganglionic cell bodies in the superior cervical ganglia of control and intoxicated rats (50 mg/kg/day for 9-10 days) with light and electron microscopy and with stereology. By light microscopy, perikarya of intoxicated rats showed peripheral Nissl bodies and nuclear eccentricity. Ultrastructurally, many experimental neurons showed augmented Nissl bodies, often extending from nucleus to plasma membrane; cisternae of granula endoplasmic bodies often appeared in orderly stacked configurations. Intoxicated neurons had increased numbers of normal-appearing mitochondria; some mitochondrial profiles appeared in clumps and others were hypertrophied. Compared to control neurons where Golgi complex most often aligned in a circumnuclear position, experimentals showed reductions in amount and loss of orientation. In some perikarya the pattern of eccentricity of nucleus, peripheral mantle of Nissl, and increased mitochondria gave a distinctive chromatolysis-like appearance. Ultrastructural stereologic analysis showed significantly increased volume fractions of Nissl (P less than 0.001) and mitochondria (P less than 0.002), a trend towards decreased Golgi, and no change in lysosomes, confirming the ultrastructural findings. These data indicate that cell body remodelling is a widespread phenomenon, specific for different neuronal types, and that it probably acts importantly in the pathogenesis of disease.

Acrylamides↗
PubMedDate not supplied

Carry over (transfer) of feed-borne acrylamide into eggs, muscle, serum, and faeces - a pilot study with Japanese quails (Coturnix coturnix japonica).

Two groups of 10 quails each were fed for 30 days on a diet containing either 663 microg feed-borne acrylamide (AA)/kg feed (group B) or 2472 microg AA/kg feed (group C) respectively. The concentrations of AA present in excreta and eggs were compared with those measured in eggs and excreta obtained from a control group (group A) fed on a diet low in AA (<10 microg/kg). The results clearly showed that the eggs of quails in group C contained approximately 53-112 microg AA/kg based on dry weight, while eggs collected from group A did not contain AA (limit of detection in eggs 3.5 microg/kg). Nearly 5% of the AA fed was recovered in the excreta. The AA concentrations in liver, muscle and serum were detectable, but below the limit of quantitation.

Acrylamide↗
PubMed1998

Poly(acrylamide-co-monoethyl itaconate) hydrogels as devices for cytarabine release in rats.

This study has tested the application of three different copolymeric poly(acrylamide-co-monoethyl itaconate; A/MEI) hydrogels, 90A/10MEI, 75A/25MEI and 60A/40MEI, on the release of cytarabine (ara-C). The drug was incorporated in gels by placing it in the polymerization feed mixture and discs loaded with 5-50 mg ara-C were obtained. The amount of swelling at equilibrium in saline solution (NaCl, 0.9% w/w) was between 78 and 82% w/w, depending on the composition of the copolymer. The diffusion studies followed Fick's second law. The diffusion coefficients for swelling of the gels were between 9.30 x 10(-11) m2 s(-1) and 37.42 x 10(-11) m2 s(-1); those for release of ara-C were between 3.42 x 10(-11) m2 s(-1) and 10.25 x 10(-11) m2 s(-1). The activation energies for swelling were in the range 16.60 +/- 2.59-21.85 +/- 1.78 kJ mol(-1); those for ara-C release were 28.13 +/- 3.1-29.7 +/- 4.6 kJ mo(-1). To determine the applicability of these copolymers, 75A/25MEI gel was subcutaneously implanted in rats and the plasma concentration of the drug was determined by high-performance liquid chromatography. The concentration of ara-C in plasma (range 17.67 +/- 5.68-10.76 +/- 2.15 microg mL(-1)) was maintained during the first stages (2-8 h) and no drug was detected after 32 h. This route of administration was compared with intraperitoneal injection of the drug. In conclusion, ara-C can be incorporated in hydrogels and released in a pharmacologically active form. The concentration of ara-C in plasma is maintained for long enough to improve therapeutic results.

Acrylamides↗