Periarteritis in Rats Given Single Injection of 4'-Fluoro-10-methyl-1,2-benzanthracene.

Hartmann, Henrik; Miller, E. C.; Miller, John A.

doi:10.3181/00379727-101-25040

Cited by 10 publications

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“…By combining with renal proteins hydrocarbons may act as haptens and induce autoimmunity against kidney cells. This mechanism was proposed by Nakajima et al in experimental DNCB nephritis [ 20 ] and may also have been operating in the experiment by Hartmann et al [ 9 ].…”

Section: Discussionmentioning

confidence: 62%

“…One experiment was reported in two papers [ 4 , 5 ], two groups used two different hydrocarbon [ 7 , 23 ]; totally 13 different hydrocarbons were used in 26 experiments. In two experiments [ 9 , 15 ] the animals were exposed to a single dose of the hydrocarbon, in the rest they were exposed intermittently. In 15 experiments, mainly the more recent ones [[ 6 , 9 , 11 - 14 , 16 - 18 , 22 , 24 - 27 ], 35], unexposed control animals or animals exposed to neutral substances were included.…”

Section: Resultsmentioning

confidence: 99%

“…In two experiments [ 9 , 15 ] the animals were exposed to a single dose of the hydrocarbon, in the rest they were exposed intermittently. In 15 experiments, mainly the more recent ones [[ 6 , 9 , 11 - 14 , 16 - 18 , 22 , 24 - 27 ], 35], unexposed control animals or animals exposed to neutral substances were included. In all of them the renal changes, if any, were mild and did not exceed those seen in normal, aging rats.…”

Section: Resultsmentioning

confidence: 99%

“…In 19 studies the tubulointerstitial tissue were described also and in all of them varying degrees of damage were noted, in particular the two experiments that produced anti-TBM nephritis[ 19 , 20 ]. Findings similar to most of the human subgroups were seen, including IgA nephritis [ 18 ], mesangial [ 13 , 16 ], crescentic [ 6 , 14 ], proliferative [ 6 , 20 ] and focal segmental proliferative [ 19 , 20 ] glomerulonephritis, focal [ 18 ], focal segmental [ 17 , 22 , 27 ] and total [ 11 , 26 ] glomerular sclerosis, minimal change nephropathy [ 11 , 20 , 25 ], anti-TBM nephritis [ 19 ] and glomerulonephritis associated with periarteritis nodosa [ 9 ]. A summary of the findings is given in Additional file 1 .…”

Section: Resultsmentioning

confidence: 99%

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Experimental glomerulonephritis induced by hydrocarbon exposure: A systematic review

Ravnskov

2005

BMC Nephrol

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BackgroundMuch epidemiological evidence suggests that hydrocarbon exposure may induce glomerulonephritis and worsen its course in many patients. The mechanisms are unknown, however, no specific microscopic pattern has been identified, and it has also been argued that hydrocarbon exposure causes tubular damage mainly. Studying experimental animals may best answer these questions, and as no systematic review of glomerulonephritis produced experimentally by hydrocarbon exposure has been performed previously, I found it relevant to search for and analyse such studies.MethodsAnimal experiments having mimicked human glomerulonephritis by hydrocarbon exposure were sought on Medline and ToxnetResultsTwenty-six experiments using thirteen different hydrocarbons were identified. Several human subtypes were observed including IgA nephritis, mesangial, proliferative and extracapillary glomerulonephritis, focal and focal-segmental sclerosis, minimal change nephropathy, anti-GBM and anti-TBM nephritis, and glomerulonephritis associated with peiarteritis nodosa. Glomerular proteinuria was seen in 10/12 experiments that included urine analyses, and renal failure in 5/8 experiments that included measurements of glomerular function. All experiments resulted in various degrees of tubular damage as well. In most studies, where the animals were examined at different times during or after the exposure, the renal microscopic and functional changes were seen immediately, whereas deposits of complement and immunoglobulins appeared late in the course, if at all.ConclusionThese experiments are in accord with epidemiological evidence that hydrocarbon exposure may cause glomerulonephritis and worsen renal function. Probable mechanisms include an induction of autologous antibodies and a disturbance of normal immunological functions. Also, tubular damage may increase postglomerular resistance, resulting in a glomerular deposition of macromolecules. In most models a causal role of glomerular immune complex formation was unlikely, but may rather have been a secondary phenomenon. As most glomerulonephritis subgroups were seen and as some of the hydrocarbons produced more than one subgroup, the microscopic findings in a patient cannot be used as a clue to the causation of his disease. By the same reason, the lack of a specific histological pattern in patients with glomerulonephritis assumed to have been caused by hydrocarbon exposure is not contradictive.

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Section: Discussionmentioning

confidence: 62%

Section: Resultsmentioning

confidence: 99%

Section: Resultsmentioning

confidence: 99%

Section: Resultsmentioning

confidence: 99%

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Experimental glomerulonephritis induced by hydrocarbon exposure: A systematic review

Ravnskov

2005

BMC Nephrol

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Biological Properties of Selected Fluorine-Containing Organic Compounds

Smith¹

1970

Pharmacology of Fluorides

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Tumor-initiating activity in mouse skin and carcinogenicity in rat mammary gland of fluorinated derivatives of benzo[a]pyrene and 3-methylcholanthrene

Cavalieri

Rogan

Higginbotham

et al. 1988

J Cancer Res Clin Oncol

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Comparative studies of tumor-initiating activity in mouse skin and carcinogenicity in rat mammary gland were conducted with benzo[a]pyrene (BP) and 3-methylcholanthrene (MC) derivatives. SENCAR mice were initiated with BP, 6-fluorobenzo[a]pyrene (6-FBP), 6-methylBP, 7-FBP, 8-FBP, 9-FBP, 10-FBP, or 10-azaBP and promoted with tetradecanoyl phorbol acetate. The same compounds plus BP 7,8-dihydrodiol were tested by intramammillary injection in female Sprague-Dawley rats. Tumor-initiating activity in mice and/or carcinogenicity in rats were observed for BP, 6-methylBP, 6-, 7-, 8-, and 10-FBP, whereas 9-FBP was inactive in both experiments and 10-azaBP was only marginally active in the mammary gland. BP 7,8-dihydrodiol was carcinogenic in rat mammary gland, although it was less potent than BP. MC, 8-FMC, 10-FMC, and 3-methylcholanthrylene were also tested in Sprague-Dawley rats by intramammillary injection. All compounds were carcinogenic, with MC displaying the most potent activity. The less potent carcinogenic activity of BP 7,8-dihydrodiol in the mammary gland, compared with BP, and the moderate-to-weak tumor-initiating and/or carcinogenic activity of 7-, 8-, and 10-FBP suggest that the bay-region diol-epoxide pathway does not play a significant role in the activation of BP in these two target tissues. Similarly, the carcinogenic activity of 8-FMC and 10-FMC, in which the bay-region diol-epoxide pathway is blocked, suggests that this mechanism of activation is not important in the carcinogenicity of MC in rat mammary gland.

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Periarteritis in Rats Given Single Injection of 4'-Fluoro-10-methyl-1,2-benzanthracene.

Cited by 10 publications

References 1 publication

Experimental glomerulonephritis induced by hydrocarbon exposure: A systematic review

Experimental glomerulonephritis induced by hydrocarbon exposure: A systematic review

Biological Properties of Selected Fluorine-Containing Organic Compounds

Tumor-initiating activity in mouse skin and carcinogenicity in rat mammary gland of fluorinated derivatives of benzo[a]pyrene and 3-methylcholanthrene

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