<scp>l</scp>-Cysteine, <i>N</i>-Acetyl-<scp>l</scp>-cysteine, and Glutathione Protect Xenopus laevis Embryos against Acrylamide-Induced Malformations and Mortality in the Frog Embryo Teratogenesis Assay

Rayburn, James R.; Friedman, Mendel

doi:10.1021/jf1023998

Cited by 40 publications

(27 citation statements)

References 46 publications

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“…After consumption, it is absorbed in the circulation and distributed to various organs, where it can react with DNA, neurons, hemoglobin, and essential enzymes (27). In the present study, we provide experimental evidence in support of the role of oxidative stress in ACR toxicity.…”

Section: Discussionsupporting

confidence: 59%

Melatonin protects against acrylamideinduced oxidative tissue damage in rats

Beceren¹

2012

mpj

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INTRODUCTION Acrylamide (CH 2 =CHCONH 2 ) is an , -unsaturated carbonyl compound with a significantly high chemical activity (1). It is extensively used mainly in the manufacture of water-soluble polymers. These polymers are primarily employed by the wastewater, paper, mining, and oil industry (2). ACR does not occur naturally. It was found in various fried, deep-fried and oven-baked foods. It occurs in foods that are regularly consumed throughout the years, not only crisps and bread, but also biscuits, crackers and breakfast cereals. Recent studies demonstrates that acrylamide can also be formed at physiological conditions (37 degrees C, pH 7.4) when asparagine is incubated in the presence of hydrogen peroxide (H 2 O 2 ). Nevertheless, it is presumably not physiologically produced in toxic concentrations (1,3).Acrylamide is toxic and an irrritant. Cases of acrylamide poisoning show signs and symptoms of local effects due to irritation of the skin and mucous membranes and systemic effects due to the involvement of the central, peripheral, and autonomic nervous systems. Studies of neurotransmitter distribution and receptor binding in the brain of rats have revealed changes induced by acrylamide. In rats, changes in the concentration of neurotransmitters and in striatal dopamine receptor binding have been related to behavioural changes. Degenerative changes in renal convoluted tubular epithelium and glomeruli and fatty degeneration and necrosis of the liver have been seen in monkeys given large doses of acrylamide. In rats, impairment of hepatic porphyrin metabolism has been observed. The toxicity of ACR is at least in part related to free radicals and free radical-mediated oxidative stress. Thus, it would be of therapeutic benefit to develop new drugs that are capable of scavenging these free radicals in the treatment of acrylamide-induced damage (4). After decapitation, liver and kidney tissues were excised. Malondialdehyde (MDA), glutathione (GSH) levels, collagen contents and myeloperoxidase activity (MPO) were determined in the tissues, while enzyme activities and cytokine levels were assayed in blood samples. In the ACR treated group, GSH levels decreased significantly while the MDA levels, MPO activity and collagen content increased in the tissues suggesting oxidative organ damage. In the MEL treated ACR group, all of these oxidant responses were reversed significantly. Serum enzyme activities, cytokine levels and leukocyte apoptosis which increased significantly following ACR administration, decreased with MEL treatment. The results demonstrate the role of oxidative mechanisms in ACR-induced tissue damage, and melatonin, by its antioxidant properties, ameliorates oxidative organ injury due to acrylamide toxicity. ABSTRACT: Acrylamide (ACR), is a widely used industrial chemical which induces

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Section: Discussionsupporting

confidence: 59%

Melatonin protects against acrylamideinduced oxidative tissue damage in rats

Beceren¹

2012

mpj

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“…30,173 The three-component study forms the basis for a novel quantitative method of defining interactions among bioactive, processing-induced food toxins. In vivo, acrylamide is reported to act as a carcinogen, neurotoxin, and reproductive toxin, whereas furan is reported to induce liver cancer in rodents, so it is also considered to be a presumptive carcinogen.…”

Section: Inhibition Of Acrylamide-induced Reproductive Toxicitymentioning

confidence: 99%

Acrylamide: inhibition of formation in processed food and mitigation of toxicity in cells, animals, and humans

Friedman

2015

Food Funct.

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Potentially toxic acrylamide is largely derived from the heat-inducing reactions between the amino group of the amino acid asparagine and carbonyl groups of glucose and fructose in plant-derived foods including cereals, coffees, almonds, olives, potatoes, and sweet potatoes. This review surveys and consolidates the following dietary aspects of acrylamide: distribution in food, exposure and consumption by diverse populations, reduction of the content in different food categories, and mitigation of adverse in vivo effects. Methods to reduce acrylamide levels include selecting commercial food with a low acrylamide content, selecting cereal and potato varieties with low levels of asparagine and reducing sugars, selecting processing conditions that minimize acrylamide formation, adding food-compatible compounds and plant extracts to food formulations before processing that inhibit acrylamide formation during processing of cereal products, coffees, teas, olives, almonds, and potato products, and reducing multiorgan toxicity (antifertility, carcinogenicity, neurotoxicity, teratogenicity). The herein described observations and recommendations are of scientific interest for food chemistry, pharmacology, and toxicology, but also have the potential to benefit nutrition, food safety, and human health.

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“…Thiol–adduct formation also reduced the very high mutagenicity of the tetrachloroimide mutagen formed in poultry chiller water [12] and inhibited the heat-induced formation in plant foods of the presumptive carcinogen and teratogen acrylamide [13,14] as well as the antinutritional compound lysinoalanine in food exposed to heat and high pH [15]. …”

Section: Aflatoxin B1 (Afb1)mentioning

confidence: 99%

Review of the Inhibition of Biological Activities of Food-Related Selected Toxins by Natural Compounds

Friedman

Rasooly

2013

Toxins

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There is a need to develop food-compatible conditions to alter the structures of fungal, bacterial, and plant toxins, thus transforming toxins to nontoxic molecules. The term ‘chemical genetics’ has been used to describe this approach. This overview attempts to survey and consolidate the widely scattered literature on the inhibition by natural compounds and plant extracts of the biological (toxicological) activity of the following food-related toxins: aflatoxin B1, fumonisins, and ochratoxin A produced by fungi; cholera toxin produced by Vibrio cholerae bacteria; Shiga toxins produced by E. coli bacteria; staphylococcal enterotoxins produced by Staphylococcus aureus bacteria; ricin produced by seeds of the castor plant Ricinus communis; and the glycoalkaloid α-chaconine synthesized in potato tubers and leaves. The reduction of biological activity has been achieved by one or more of the following approaches: inhibition of the release of the toxin into the environment, especially food; an alteration of the structural integrity of the toxin molecules; changes in the optimum microenvironment, especially pH, for toxin activity; and protection against adverse effects of the toxins in cells, animals, and humans (chemoprevention). The results show that food-compatible and safe compounds with anti-toxin properties can be used to reduce the toxic potential of these toxins. Practical applications and research needs are suggested that may further facilitate reducing the toxic burden of the diet. Researchers are challenged to (a) apply the available methods without adversely affecting the nutritional quality, safety, and sensory attributes of animal feed and human food and (b) educate food producers and processors and the public about available approaches to mitigating the undesirable effects of natural toxins that may present in the diet.

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l-Cysteine, N-Acetyl-l-cysteine, and Glutathione Protect Xenopus laevis Embryos against Acrylamide-Induced Malformations and Mortality in the Frog Embryo Teratogenesis Assay

Cited by 40 publications

References 46 publications

Melatonin protects against acrylamideinduced oxidative tissue damage in rats

Melatonin protects against acrylamideinduced oxidative tissue damage in rats

Acrylamide: inhibition of formation in processed food and mitigation of toxicity in cells, animals, and humans

Review of the Inhibition of Biological Activities of Food-Related Selected Toxins by Natural Compounds

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