Acute intraperitoneal toxicity of ochratoxin a and B derivatives in rainbow trout (Salmo gairdneri)

Doster, R.C.; Sinnhuber, R. O.; Pawlowski, Norman E.

doi:10.1016/0015-6264(74)90063-7

Cited by 29 publications

(23 citation statements)

References 8 publications

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“…Interestingly, primary cells have been demonstrated to be more susceptible to the cytotoxic effects of both OTA and OTB when crystal violet staining of intact nuclei is taken as MTT reduction (% control) no effect limit 30% effect limit MTT reduction (% control) no effect limit 30% effect limit MTT reduction (% control) no effect limit endpoint , whereas this was not apparent via assessment of other endpoints . OTB has often been reported to be less toxic than OTA in vivo (Doster et al, 1972(Doster et al, , 1974Stør-mer et al, 1985) and in vitro. However, more recent in vitro data brings this into question (Mally et al, 2005).…”

Section: Discussionmentioning

confidence: 99%

In vitro investigation of individual and combined cytotoxic effects of ochratoxin A and other selected mycotoxins on renal cells

Heussner

Dietrich

O'Brien

2006

Toxicology in Vitro

103

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Hundreds of mycotoxins are known to date and many of them are of great interest with regard to human and animal health since they are detected frequently in plant-derived products. Various mycotoxins may occur simultaneously, depending on the environmental and substrate conditions. Considering this coincident production, it is very likely, that humans and animals are always exposed to mixtures rather than to individual compounds. Therefore, future risk assessments should consider mixture toxicity data. This is particularly true for ochratoxin A (OTA), ochratoxin B (OTB), citrinin (CIT) and occasionally for patulin (PAT) as they are all produced by a number of Penicillium and Aspergillus species. Therefore, these four toxins were chosen to study the interactive effects in vitro, using the well-established porcine renal cell line LLC-PK1 and the MTT reduction test as a cytotoxicity endpoint. By application of a step-wise approach to test combination toxicity, using various full factorial as well as a central composite experimental designs, the interactive (synergistic) cytotoxic effects of the these four toxins were assessed. The results obtained in this study confirm a potential for interactive (synergistic) effects of CIT and OTA and possibly other mycotoxins in cells of renal origin.

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Section: Discussionmentioning

confidence: 99%

In vitro investigation of individual and combined cytotoxic effects of ochratoxin A and other selected mycotoxins on renal cells

Heussner

Dietrich

O'Brien

2006

Toxicology in Vitro

103

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“…Dosing of F344 rats with low (21-210 µg OTA/ kg bw) for 2 years produced a ten-fold higher incidence of renal cortical tumors in male than in female rats (BOORMAN 1989). A similar carcinogenicity study conducted with B6C3F 1 mice, however using up to 4 mg OTA/ kg bw, produced a 62% incidence of renal toxic in vivo (DOSTER et al 1972;PECKHAM et al 1971). Therefore, OTA and OTB were used for comparison in all tests.…”

Section: Introductionmentioning

confidence: 99%

Species- and sex-specific renal cytotoxicity of Ochratoxin A and B in vitro

Dietrich

O'Brien

Stack

et al. 2001

Experimental and Toxicologic Pathology

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SummaryFour different cell models were chosen for comparison of OTA and OTB toxicity: primary porcine (PKC), rat (RPTC) and human renal proximal epithelial cells (HKC) from both sexes and a porcine renal cell line: LLC-PK1. Culture conditions were tested and optimized for each respective cell type (species/sex and origin). All cell types were characterized for epithelial origin and growth patterns and following optimization of dosing strategies and assay procedures, a strict study design was implemented to avoid systemic variations. Due to possible sensitivity differences, three simple endpoints were chosen to provide basic data for interspecies comparison: neutral red uptake, MTT reduction and cell number. Of the endpoints tested neutral red appeared the most sensitive, although all three parameters yielded comparable EC 50 's. Sex-differences were observed between male and female HKC cells following 96 h exposure to OTA, with HKC(m) being more sensitive than HKC(f). No sex-difference was observed in PKC cells, however, the PKC were approximately 3 and 10 times more sensitive than HKC(m) and HKC(f), respectively, to OTA and OTB. Interestingly, the CI 95 of the EC 50 values obtained for OTA (15.5-16.5 µM) and OTB (17.0-21.0 µM) were comparable in the PKC cells. In contrast, OTB had lower cytotoxicity than OTA in HKC and LLC-PK1 (approx. 2-fold) and no effects in RPTC. Overall, HKC(m) were nearly as sensitive as PKC towards OTA, followed by RPTC, LLC-PK1 and HKC(f), thus suggesting a sex specific sensitivity in humans towards OTA induced cytotoxicity.

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“…Pathologic changes induced by ochratoxin A in several species including the rat [19, 20, 23, 24, 27, 281, pig [14][15][16]251, rainbow trout [9], dog [26], duckling [22, 271, chick [6,10,211 and hen [4] have been described. Changes included renal tubular necrosis, hepatic and lymphoid necrosis and intestinal ulceration.…”

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Ochratoxin A and Citrinin Induced Nephrosis in Beagle Dogs II. Pathology

1977

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Abstract. Beagle dogs were given ochratoxin A (0.1 and 0.2 mg/kg) and citrinin ( 5 and 10 mg/kg) alone and in two dose combinations for 14 days. The gross lesions included focal peritonitis and intestinal intussusceptions in dogs given citrinin. Changes in the kidneys of dogs given ochratoxin A were degeneration and necrosis with desquamation of tubular epithelial cells, primarily in the straight segment of the proximal tubules. Dogs given 10 mg/kg citrinin had similar changes in the distal tubules and collecting ducts. Dogs given combined doses of citrinin and ochratoxin A had degeneration and necrosis in proximal and distal tubules, and in thin segments and the collecting ducts; there were desquamated cells and granular casts in the lumina. Dogs given ochratoxin A had necrosis of lymphoid tissues in the spleen, tonsil, thymus, peripheral lymph nodes and lymph nodules of the ileum, colon and rectum. There was ulceration of the mucosa of the intestine in dogs given large combined doses of ochratoxin A and citrinin.The clinical and clinicopathologic features of the mycotoxicoses produced in Beagle dogs by administration of ochratoxin A and citrinin alone and in combination have been described [13]. Pathologic changes induced by ochratoxin A in several species including the rat [19, 20, 23, 24, 27, 281, pig [14][15][16] 251 [22, 271, chick [6, 10, 211 and hen [4] have been described. Changes included renal tubular necrosis, hepatic and lymphoid necrosis and intestinal ulceration.In previous reports of citrinin toxicosis the proximal convoluted tubules of kidneys were changed in all species studied [1, 21. In the dog, renal lesions of citrinin toxicosis included degeneration and necrosis of the tubular epithelium, primarily of the straight segments and distal convoluted tubules [ 3 ] .This report describes changes in dogs given ochratoxin A , citrinin and the two mycotoxins in combination. Materials and MethodsThirty five 10-week-old male Beagle dogs were purchased for the six trials of this study. They were given daily oral doses of either ochratoxin A or daily intraperitoneal injections of citrinin dissolved in absolute ethanol or in combination, according to the dosage regimen in table I. Control dogs were dosed with ethanol. The dogs were housed in metabolism cages and blood was taken periodically for 261

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Acute intraperitoneal toxicity of ochratoxin a and B derivatives in rainbow trout (Salmo gairdneri)

Cited by 29 publications

References 8 publications

In vitro investigation of individual and combined cytotoxic effects of ochratoxin A and other selected mycotoxins on renal cells

In vitro investigation of individual and combined cytotoxic effects of ochratoxin A and other selected mycotoxins on renal cells

Species- and sex-specific renal cytotoxicity of Ochratoxin A and B in vitro

Ochratoxin A and Citrinin Induced Nephrosis in Beagle Dogs II. Pathology

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