On the histopathogenesis of rat forestomach carcinoma caused by aristolochic acid

Mengs, U.

doi:10.1007/bf00333900

Cited by 95 publications

(38 citation statements)

References 28 publications

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“…The similar levels of DNA adducts achieved in renal cortex, medulla, and bladder in mice treated with equivalent doses of AA-I and AA-II suggest that each toxin produces similar degrees of DNA damage in renal proximal tubules and urothelial cells. Assuming that the mutagenic potentials of AA-I-and AA-II-derived DNA adducts are similar, either AA-I or AA-II might initiate the cancers associated with AAN (Arlt et al, 2002;Mengs, 1983Mengs, , 1988Cui et al, 2005).…”

Section: Discussionmentioning

confidence: 99%

“…Toxicologic studies in mice, rats, and rabbits reveal that treatment with AA is associated with renal tubular damage (Mengs and Stotzem, 1993;Cosyns et al, 2001), interstitial fibrosis (Cosyns et al, 2001;Debelle et al, 2002), and cancer Mengs, 1983Mengs, , 1988Cui et al, 2005). Cosyns et al (2001) used a rabbit model to study the toxicities of AAs by injecting an i.p.…”

mentioning

confidence: 99%

“…The proposed use of AAs as a therapeutic agent was largely abandoned when Mengs (1983) demonstrated their carcinogenicity in rats. Mengs (1988) subsequently reported the formation of tumors in multiple organs when mice were treated with a mixture of AA-I and AA-II at a dose of 5.0 mg/kg/day for 3 weeks.…”

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confidence: 99%

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Selective Toxicity of Aristolochic Acids I and II

Shibutani

Dong²,

Suzuki³

et al. 2007

Drug Metab Dispos

138

124

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ABSTRACT:Ingestion of herbal remedies containing aristolochic acids (AAs) is associated with the development of a syndrome, designated aristolochic acid nephropathy (AAN), which is characterized by chronic renal failure, tubulointerstitial fibrosis, and urothelial cancer. To distinguish the component(s) of AA responsible for these varied toxic effects, we administered 2.5 mg/kg/day of AA-I or AA-II for 9 days, either i.p. or p.o., to male C3H/He mice. Tissues were then collected and subjected to biochemical and histopathologic examination. Genotoxicity was assessed by determining quantitatively the level of aristolactam-DNA adducts in various tissues using 32 P-postlabeling/polyacrylamide gel electrophoresis and an internal standard. In the primary target tissues, represented by the renal cortex, medulla, and bladder, we found similar levels of DNA adducts derived from AA-I and AA-II. However, in nontarget tissues, the liver, stomach, intestine, and lung, the levels of aristolactam-DNA adducts derived from AA-I were significantly higher than those derived from AA-II. Histopathologic analysis revealed tubular cell necrosis and interstitial fibrosis in the renal cortex of AA-I-treated mice but only minimal changes in the renal cortex of mice treated with AA-II. We conclude that AA-I and AA-II have similar genotoxic and carcinogenic potential, and, although both compounds are cytotoxic, AA-I is solely responsible for the nephrotoxicity associated with AAN.

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Section: Discussionmentioning

confidence: 99%

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confidence: 99%

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Selective Toxicity of Aristolochic Acids I and II

Shibutani

Dong²,

Suzuki³

et al. 2007

Drug Metab Dispos

138

124

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“…Efforts to exploit the anti-inflammatory and antitumor properties of AA were halted after it was shown to be mutagenic and carcinogenic (2,41). Aristolochic acid nephropathy (AAN) was first described among clients of a Belgian weight loss clinic inadvertently treated with an herbal mixture containing extracts of A. fangchi (65).…”

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confidence: 99%

Genetic loci that affect aristolochic acid-induced nephrotoxicity in the mouse

Rosenquist

2011

American Journal of Physiology-Renal Physiology

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“…It is conceivable that these changes were induced by CMP inhalation. It has been suggested that epithelial hyperplasia of the forestomach may progress to become a papilloma, and subsequently a carcinoma, in many previous reports 3,[9][10][11][12][13][14][15][16] . In the present study, it was similarly suggested that the neoplastic lesions of the forestomach progressed with such a pattern.…”

Section: Discussionmentioning

confidence: 99%

Chronic Ihhalation Toxicity and Carcinogenicity Studies of 3-Chloro-2-methylpropene in BDF1 Mice.

Katagiri¹,

Takeuchi²,

Mine³

et al. 2000

INDUSTRIAL HEALTH

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Chronic toxicity and carcinogenicity studies of 3-chloro-2-methylpropene (CMP), which has been widely used as an insecticide and chemical intermediate, were carried out in BDF1 mice. CMP was administered to mice in groups of 50 male and 50 female mice by the inhalation route 5 days per week for 104 weeks at doses of 0, 50, 100 or 200 ppm. Male and female mice in the CMPexposed groups had decreased body weight but no noticeable clinical signs when compared with the control group. Dose-related increases in the incidences of gastric mucosal hyperplasia and squamous cell papilloma were observed in both sexes, and squamous cell carcinoma was observed in only one male mouse in the 100 ppm group. An increased incidence of Harderian gland adenoma in female mice was also recognized. In the nasal cavity, eosinophilic exudate associated with atrophy of olfactory epithelia, respiratory metaplasia of olfactory epithelia and olfactory gland, and eosinophilic changes in respiratory and olfactory epithelia were increased in both sexes.

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On the histopathogenesis of rat forestomach carcinoma caused by aristolochic acid

Cited by 95 publications

References 28 publications

Selective Toxicity of Aristolochic Acids I and II

Selective Toxicity of Aristolochic Acids I and II

Genetic loci that affect aristolochic acid-induced nephrotoxicity in the mouse

Chronic Ihhalation Toxicity and Carcinogenicity Studies of 3-Chloro-2-methylpropene in BDF1 Mice.

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