Intestinal effects of carrageenans in the rhesus monkey (Macaca mulatta)

Benitz, K.-F.; Golberg, L.; Coulston, F.

doi:10.1016/s0015-6264(73)80327-x

Cited by 85 publications

(26 citation statements)

References 14 publications

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“…Two males and two females were allowed an 11-week recovery period and were then given carrageenan at escalating oral doses of 50-1250 mg/kg bw per day for up to 12 weeks. No gross adverse effects were observed, and the microscopic changes were not attributed to carrageenan (Benitz et al 1973). Male and female infant baboons were reared from birth to 112 days of age on infant formula containing 0, 1, or 5% kappa/lambda-carrageenan derived from C. crispus.…”

Section: Short-term Studies Of Toxicitymentioning

confidence: 99%

Carrageenan: a review

Nečas¹,

2013

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Carrageenan is a natural carbohydrate (polysaccharide) obtained from edible red seaweeds. The name Carrageenan is derived from the Chondrus crispus species of seaweed known as Carrageen Moss or Irish Moss in England, and Carraigin in Ireland. Carraigin has been used in Ireland since 400 AD as a gelatin and as a home remedy to cure coughs and colds. It grows along the coasts of North America and Europe. Carrageenans are used in a variety of commercial applications as gelling, thickening, and stabilising agents, especially in food products and sauces. Aside from these functions, carrageenans are used in experimental medicine, pharmaceutical formulations, cosmetics, and industrial applications.Keywords: carrageenan; pharmacokinetics; toxicity; biological activity List of abbreviations 3,6-AG = 3,6, anhydro-galactose, 5-HT = 5-hydroxytryptamine, 6-APA = 6-amino penicillanic acid, ADI = acceptable daily intake, AG = amino guanidine, AIDS = acquired immune deficiency syndrome, AT-III = anti-thrombin-III, bw = body weight, COX-2 = cyclooxygenase-2, eNOS = endothelial nitric oxide synthase, FAO = food and agriculture organization, HC-II = heparin co-factor II, HIV = human immunodeficiency virus, HPV = human papilloma virus, HSV = herpes simplex virus, IFAC = international food additives council, iNOS = inducible nitric oxide synthase, JECFA = Joint FAO/WHO Expert Committee on Food Additives, L-NMMA = NG-monomethyl-l-arginine, nNOS = neuronal nitric oxide synthase, NO = nitric oxide, NOS = nitric oxide synthase, NSAIDs = non-steroidal antiinflammatory drugs, PGs = prostaglandins, SSL = sodium stearoyl lactylate, TNF-α = tumour necrosis factor-α

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Section: Short-term Studies Of Toxicitymentioning

confidence: 99%

Carrageenan: a review

Nečas¹,

2013

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“…CGNs are derived by alkaline extraction from red seaweed (Rhodophycae) and structurally mimic the naturally occurring sulfated glycosaminoglycans (6). Multiple studies in mammals have demonstrated that CGN ingestion causes adverse effects on the intestine, including development of ulcerations, polyps, colitis, and colorectal tumors, and predictably induces inflammation in other sites in animal models, including in pleura, peritoneum, hind paw, and subcutaneous blebs (1)(2)(3)(7)(8)(9)(10).…”

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confidence: 99%

Tumor Necrosis Factor α-induced Inflammation Is Increased but Apoptosis Is Inhibited by Common Food Additive Carrageenan

Bhattacharyya

Dudeja

Tobacman

2010

Journal of Biological Chemistry

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Tumor necrosis factor (TNF)-␣, a homotrimeric, pleiotropic cytokine, is secreted in response to inflammatory stimuli in diseases such as rheumatoid arthritis and inflammatory bowel disease. TNF-␣ mediates both apoptosis and inflammation, stimulating an inflammatory cascade through the non-canonical pathway of NF-B activation, leading to increased nuclear RelB and p52. In contrast, the common food additive carrageenan (CGN) stimulates inflammation through both the canonical and non-canonical pathways of NF-B activation and utilizes the adaptor molecule BCL10 (B-cell leukemia/lymphoma 10). In a series of experiments, colonic epithelial cells and mouse embryonic fibroblasts were treated with TNF-␣ and carrageenan in order to simulate the possible effects of exposure to dietary CGN in the setting of a TNF-␣-mediated inflammatory disease process. A marked increase in secretion of IL-8 occurred, attributable to synergistic effects on phosphorylated NF-B-inducing kinase (NIK) in the non-canonical pathway. TNF-␣ induced the ubiquitination of TRAF2 (TNF receptor-associated factor 2), which interacts with NIK, and CGN induced phosphorylation of BCL10, leading to increased NIK phosphorylation. These results suggest that TNF-␣ and CGN in combination act to increase NIK phosphorylation, thereby increasing activation of the non-canonical pathway of NF-B activation. In contrast, the apoptotic effects of TNF-␣, including activation of caspase-8 and PARP-1 (poly(ADP-ribose) polymerase 1) fragmentation, were markedly reduced in the presence of CGN, and CGN caused reduced expression of Fas. These findings demonstrate that exposure to CGN drives TNF-␣-stimulated cells toward inflammation rather than toward apoptotic cell death and suggest that CGN exposure may compromise the effectiveness of anti-TNF-␣ therapy. Carrageenan (CGN),2 a polysaccharide composed of sulfated galactose residues in ␣-1,3 and ␤-1,4 linkages, has been widely used for decades as a thickener, stabilizer, or emulsifying agent in many processed food products in the Western diet, including in dairy products (chocolate milk, ice cream, cottage cheese, yogurt, etc.), processed meats, soymilk, and infant formula. It is also widely used in a variety of non-food products, including cosmetics, toothpaste, room deodorizers, and pharmaceuticals (1-3). Current data suggest average consumption of 250 mg/day in the United States (5) (see the Encyclopaedia Britannica Online Web site). CGNs are derived by alkaline extraction from red seaweed (Rhodophycae) and structurally mimic the naturally occurring sulfated glycosaminoglycans (6). Multiple studies in mammals have demonstrated that CGN ingestion causes adverse effects on the intestine, including development of ulcerations, polyps, colitis, and colorectal tumors, and predictably induces inflammation in other sites in animal models, including in pleura, peritoneum, hind paw, and subcutaneous blebs (1-3, 7-10).Investigation of CGN-related inflammatory processes in human colonic cell lines has demonstrated that CGN induces NF-B ...

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“…When the Food and Drug Administration (FDA) considered the status of carrageenan in the early 1970s, their review included a study of 24 rhesus monkeys with appropriate controls (4,5). Investigators observed that monkeys fed 2% degraded carrageenan did not gain weight, had an immediate change in stool consistency, and consistently had blood in their stools, which was associated with a decline in hemoglobin, until approximately 10 weeks after the withdrawal of the carrageenan.…”

Section: Carrageenan In Foods: Responsementioning

confidence: 99%

“…The safety of carrageenan for use in foods was confirmed at the 57th meeting of the Joint Food and Agriculture Organization of the United Nations/World Health Organization Expert Committee on Food Additives (JECFA) in Rome in June 2001 (5). The JECFA recommended an acceptable daily intake (ADI) of "not specified," the most favorable ADI for a food additive.…”

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confidence: 99%

Carrageenan in Foods: Response

Tobacman¹

2002

Environ Health Perspect

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Intestinal effects of carrageenans in the rhesus monkey (Macaca mulatta)

Cited by 85 publications

References 14 publications

Carrageenan: a review

Carrageenan: a review

Tumor Necrosis Factor α-induced Inflammation Is Increased but Apoptosis Is Inhibited by Common Food Additive Carrageenan

Carrageenan in Foods: Response

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