The potent colon carcinogen, 1,2-dimethylhydrazine induces mutations primarily in the colon

Newell, Lórien E.; Heddle, John A.

doi:10.1016/j.mrgentox.2004.06.005

Cited by 65 publications

(47 citation statements)

References 12 publications

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“…DMH also induces point mutations, micronuclei, and sister chromatid exchanges, and produces free radicals (Sengottuvelan et al 2006). These lead to apoptosis of colonocytes and stimulate cell proliferation, which causes the appearance of precancerous lesions in the colon tissue (Newell and Heddle 2004).To determine the effects of B. cuspidata on the hepatic antioxidant enzymes in the rats after the induction of the ACF with DMH, the CAT and SOD activities were measured. The DMSO, B200, and B400 groups presented lower SOD activity than the saline group, indicating that the DMSO and extract protected the liver and prevented increased expression of SOD, probably by suffering less tissue destruction by the action of free radicals that were generated by the application of DMH.…”

Section: Discussionmentioning

confidence: 99%

Extract of the Bark of Bathysa cuspidataAttenuates the Development of Chemically-Induced Preneoplastic Colorectal Lesions in Rats

Rosa

Reis

Siqueira

et al. 2015

Braz. arch. biol. technol.

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Section: Discussionmentioning

confidence: 99%

Extract of the Bark of Bathysa cuspidataAttenuates the Development of Chemically-Induced Preneoplastic Colorectal Lesions in Rats

Rosa

Reis

Siqueira

et al. 2015

Braz. arch. biol. technol.

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“…1, 2 Dimethyl hydrazine (DMH), is a potent colon carcinogen, inducing colorectal tumors in experimental animals (Newell and Heddle, 2004;Saini et al, 2009) and is the most widely used model of chemically induced colon carcinogenesis. DMH induced colon cancer is a multistep process involving a series of pathological alterations, such as formation of aberrant cryptic foci (discrete microscopic lesion; Ionov et al, 1993).…”

Section: Introductionmentioning

confidence: 99%

Amelioration of 1,2 Dimethylhydrazine (DMH) Induced Colon Oxidative Stress, Inflammation and Tumor Promotion Response by Tannic Acid in Wistar Rats

Hamiza¹,

Rehman²,

Tahir³

et al. 2012

Asian Pacific Journal of Cancer Prevention

100

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Colon cancer is the third most common malignant neoplasm in the world and it remains an important cause of death, especially in western countries. The toxic environmental pollutant, 1, 2-dimethylhydrazine (DMH), is also a colon-specific carcinogen. Tannic acid (TA) is reported to be effective against various types of chemically induced toxicity and also carcinogenesis. In the present study, we evaluated the chemopreventive efficacy of TA against DMH induced colon toxicity in a rat model. Efficacy of TA against the colon toxicity was evaluated in terms of biochemical estimation of antioxidant enzyme activities, lipid peroxidation, histopathological changes and expression of early molecular markers of inflammation and tumor promotion. DMH treatment induced oxidative stress enzymes (p<0.001) and an early inflammatory and tumor promotion response in the colons of Wistar rats. TA treatment prevented deteriorative effects induced by DMH through a protective mechanism that involved reduction of oxidative stress as well as COX-2, i-NOS, PCNA protein expression levels and TNF-α (p<0.001) release. It could be concluded from our results that TA markedly protects against chemically induced colon toxicity and acts plausibly by virtue of its antioxidant, anti-inflammatory and antiproliferative activities.

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“…However, this compound is both a strong promoter and weak initiator of carcinogenesis. DMH is an indirect agent; in other words, it requires enzymes to convert it into an electrophilic species that will bind DNA (Newell and Heddle, 2004) and thus promote the formation of methyl group adducts, point mutations, and sister chromatid breakage (Newell and Heddle, 2004), which can then be evaluated by the alkaline (pH > 13) version of the comet assay, as performed in this study. This assay detects direct damage, including single and double-strand breaks, alkali-labile sites, crosslinks, and excision repair sites, as well as indirect damage, including methylation and adduct lesions, which are alkali-labile and appear as simple breaks under alkali treatment (Vieira et al, 2014).…”

Section: Discussionmentioning

confidence: 99%

Genomic lesions and colorectal carcinogenesis: the effects of protein-calorie restriction and inulin supplementation on deficiency statuses

Cantero¹,

Takahachi²,

Mauro³

et al. 2015

Genet. Mol. Res.

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ABSTRACT. The present study investigated the effects of restricting protein and calories and supplementation of inulin, a fiber comprising a linear type of polydisperse carbohydrates composed primarily of 2423 ©FUNPEC-RP www.funpecrp.com.br Genetics and Molecular Research 14 (1): 2422-2435 (2015) Inulin prevents cancer in malnourished animals fructil-fructose bonds (β-(2→1), on the deficiency statuses of animals in which genomic lesion development and colorectal carcinogenesis had been induced. This experiment involved adult male Swiss mice (N = 11/group). The experimental groups were as follows: Negative Control (vehicle), Positive Control, 1,2-dimethylhydrazine (DMH), Inulin, and Associate. DMH, which promoted colorectal cancer, was administered intraperitoneally in 4 20-mg/kg body weight (bw) doses during a 2-week period; inulin was administered orally at a daily dose of 50 mg/kg bw. Each group was bifurcated; half of each group was fed a normal protein diet and the other half was fed a low-protein diet. The results indicated that a correlation existed between malnutrition and an increased frequency of genomic lesions but that malnutrition did not predispose animals to colorectal cancer development. Inulin exhibited genotoxic activity, which requires further investigation, and low antigenotoxic activity. Moreover, inulin reduced the levels of intestinal carcinogenesis biomarkers in both malnourished and healthy animals. These data suggest that inulin holds therapeutic potential and is a strong candidate for inclusion among the functional foods used for cancer prevention in both properly nourished and malnourished individuals.

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The potent colon carcinogen, 1,2-dimethylhydrazine induces mutations primarily in the colon

Cited by 65 publications

References 12 publications

Extract of the Bark of Bathysa cuspidataAttenuates the Development of Chemically-Induced Preneoplastic Colorectal Lesions in Rats

Extract of the Bark of Bathysa cuspidataAttenuates the Development of Chemically-Induced Preneoplastic Colorectal Lesions in Rats

Amelioration of 1,2 Dimethylhydrazine (DMH) Induced Colon Oxidative Stress, Inflammation and Tumor Promotion Response by Tannic Acid in Wistar Rats

Genomic lesions and colorectal carcinogenesis: the effects of protein-calorie restriction and inulin supplementation on deficiency statuses

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