Response of Laboratory Animals to Cellulose Glycolic Acid and Its Sodium and Aluminum Salts

Rowe, V. K.; Spencer, Howard C.; Adams, Eliane; Irish, D. D.

doi:10.1111/j.1365-2621.1944.tb16675.x

Cited by 18 publications

(4 citation statements)

References 1 publication

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“…We have to admit that there is a deficiency in our study: although a number of animal studies have pointed out that CMC has no effect on histopathological and biochemical changes, 50 , 51 , 52 compared with normal saline, the mice in NC group using 0.5% CMC as control would be a better choice.…”

Section: Discussionmentioning

confidence: 99%

Pirfenidone modulates macrophage polarization and ameliorates radiation‐induced lung fibrosis by inhibiting the TGF‐β1/Smad3 pathway

Ying

Fang

Hang

et al. 2021

J Cellular Molecular Medi

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Radiation‐induced lung injury (RILI) mainly contributes to the complications of thoracic radiotherapy. RILI can be divided into radiation pneumonia (RP) and radiation‐induced lung fibrosis (RILF). Once RILF occurs, patients will eventually develop irreversible respiratory failure; thus, a new treatment strategy to prevent RILI is urgently needed. This study explored the therapeutic effect of pirfenidone (PFD), a Food and Drug Administration (FDA)‐approved drug for (IPF) treatment, and its mechanism in the treatment of RILF. In vivo, C57BL/6 mice received a 50 Gy dose of X‐ray radiation to the whole thorax with or without the administration of PFD. Collagen deposition and fibrosis in the lung were reversed by PFD treatment, which was associated with reduced M2 macrophage infiltration and inhibition of the transforming growth factor‐β1 (TGF‐β1)/Drosophila mothers against the decapentaplegic 3 (Smad3) signalling pathway. Moreover, PFD treatment decreased the radiation‐induced expression of TGF‐β1 and phosphorylation of Smad3 in alveolar epithelial cells (AECs) and vascular endothelial cells (VECs). Furthermore, IL‐4–induced M2 macrophage polarization and IL‐13–induced M2 macrophage polarization were suppressed by PFD treatment in vitro, resulting in reductions in the release of arginase‐1 (ARG‐1), chitinase 3‐like 3 (YM‐1) and TGF‐β1. Notably, the PFD‐induced inhibitory effects on M2 macrophage polarization were associated with downregulation of nuclear factor kappa‐B (NF‐κB) p50 activity. Additionally, PFD could significantly inhibit ionizing radiation‐induced chemokine secretion in MLE‐12 cells and consequently impair the migration of RAW264.7 cells. PFD could also eliminate TGF‐β1 from M2 macrophages by attenuating the activation of TGF‐β1/Smad3. In conclusion, PFD is a potential therapeutic agent to ameliorate fibrosis in RILF by reducing M2 macrophage infiltration and inhibiting the activation of TGF‐β1/Smad3.

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Section: Discussionmentioning

confidence: 99%

Pirfenidone modulates macrophage polarization and ameliorates radiation‐induced lung fibrosis by inhibiting the TGF‐β1/Smad3 pathway

Ying

Fang

Hang

et al. 2021

J Cellular Molecular Medi

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“…In another study, 10 female Wistar rats with an age of 82-98 days were fed a diet containing 20% CMC (equivalent to 18,000 mg/kg bw per day) for 63 days (Rowe et al, 1943). All animals were weighed twice weekly and individual weight records were kept throughout the experimental period.…”

Section: Ratsmentioning

confidence: 99%

“…Data on acute oral toxicity were available for microcrystalline cellulose, powdered cellulose, ethyl cellulose, hydroxypropyl cellulose, hydroxypropyl methyl cellulose and sodium carboxy methyl cellulose. Apart from one unpublished study with hydroxypropyl methyl cellulose, where an oral LD 50 value of > 1,000 mg/kg bw was given for rats (CTFA, ), the oral LD 50 values for the different other celluloses were consistently ≥ 3,000 mg/kg bw (Documentation provided to EFSA n. 20, 25, Freeman, ; referred to by JECFA, ,b, ,b, Palotta, ; referred to by JECFA, ,b, ,b, Rowe et al., ; Shelanski and Clark, ; Industrial Bio‐Test Lab, ; Kitagawa et al., , ; Moreno, ). Therefore, the Panel considered the oral acute toxicity of these compounds to be low.…”

Section: Biological and Toxicological Datamentioning

confidence: 99%

Re‐evaluation of celluloses E 460(i), E 460(ii), E 461, E 462, E 463, E 464, E 465, E 466, E 468 and E 469 as food additives

Younes¹,

Aggett²,

Aguilar³

et al. 2018

EFS2

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Following a request from the European Commission, the EFSA Panel on Food Additives and Nutrient Sources added to Food (ANS) was asked to deliver a scientific opinion re-evaluating the safety of microcrystalline cellulose (E 460(i)), powdered cellulose (E 460(ii)), methyl cellulose (E 461), ethyl cellulose (E 462), hydroxypropyl cellulose (E 463), hydroxypropyl methyl cellulose (E 464), ethyl methyl cellulose (E 465), sodium carboxy methyl cellulose (E 466), enzymatically hydrolysed carboxy methyl cellulose (E 469) and cross-linked carboxy methyl cellulose (E 468) as food additives. The Joint FAO/WHO Expert Committee on Food Additives (JECFA) and the Scientific Committee on Food (SCF) established an acceptable daily intake (ADI) 'not specified' for unmodified and modified celluloses. Celluloses are not absorbed and are excreted intact in the faeces; in addition, microcrystalline cellulose, powdered and modified celluloses could be fermented by the intestinal flora in animals and humans. Specific toxicity data were not always available for all the celluloses evaluated in the present opinion and for all endpoints. Given their structural, physicochemical and biological similarities, the Panel considered it possible to readacross between all the celluloses. The acute toxicity of celluloses was low and there was no genotoxic concern. Short-term and subchronic dietary toxicity studies performed with E 460(i), E 461, E 462, E 463, E 464, E 466 and E 469 at levels up to 10% did not indicate specific treatment related adverse effects. In chronic toxicity studies performed with E 460(i), E 461, E 463, E 464, E 465 and E 466, the no observed adverse effect level (NOAEL) values reported ranged up to 9,000 mg/kg body weight (bw) per day. No carcinogenic properties were detected for microcrystalline cellulose and modified celluloses. Adverse effects on reproductive performance or developmental effects were not observed with celluloses at doses greater than 1,000 mg/kg bw by gavage (often the highest dose tested). The combined exposure to celluloses (E 460-466, E 468 and E 469) at 95th percentile of the refined (brand-loyal) exposure assessment for the general population was up to 506 mg/kg bw per day. The Panel concluded that there was no need for a numerical ADI and that there would be no safety concern at the reported uses and use levels for the unmodified and modified celluloses (E 460(i); E 460(ii); E 461-466; E 468 and E 469). The Panel considered an indicative total exposure of around 660-900 mg/kg bw per day for microcrystalline, powdered and modified celluloses.

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“…Werle (1941) also showed that sodium carboxymethylcellulose was harmless physiologically when fed to rats and dogs for a two-month period. Rowe, Spencer, Adams, and Irish (1944) have shown in their work with rats that sodium carboxymethylcellulose is harmless physiologically and that there is no evidence why these materials should not be incorporated into food for human consumption.…”

mentioning

confidence: 99%

Physiological Action Op Sodium Carboxymethyl‐cellulose on Laboratory Animals and Humans

Shelanski¹,

Clark²

1948

Journal of Food Science

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Response of Laboratory Animals to Cellulose Glycolic Acid and Its Sodium and Aluminum Salts

Cited by 18 publications

References 1 publication

Pirfenidone modulates macrophage polarization and ameliorates radiation‐induced lung fibrosis by inhibiting the TGF‐β1/Smad3 pathway

Pirfenidone modulates macrophage polarization and ameliorates radiation‐induced lung fibrosis by inhibiting the TGF‐β1/Smad3 pathway

Re‐evaluation of celluloses E 460(i), E 460(ii), E 461, E 462, E 463, E 464, E 465, E 466, E 468 and E 469 as food additives

Physiological Action Op Sodium Carboxymethyl‐cellulose on Laboratory Animals and Humans

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