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Pagina 1 a partire dal 18 risultati
The mycotoxins citrinin and gliotoxin differentially affect production of the pro-inflammatory cytokines tumour necrosis factor-alpha and interleukin-6, and the anti-inflammatory cytokine interleukin-10.
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BACKGROUND
Microbial growth is considered one of the major causes of indoor air problems. Moulds have been associated with asthma, allergy and a wide range of diffuse indoor air-related symptoms. However, mechanisms of the adverse health effects are not well understood.
OBJECTIVE
We hypothesized
Evaluation of citrinin-induced toxic effects on mouse Sertoli cells.
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Penicillium citrinum-derived mycotoxin citrinin (CTN) is known to be a toxic agent for humans and animals. Previous studies have shown that CTN leads to toxicity in many biological systems; however, a limited number of studies have been performed to demonstrate the harmful effects of CTN on
The effects of potassium chromate and citrinin on rat renal membrane transport.
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Both chromate and citrinin have been shown to produce acute renal damage. Although both substrates act on the proximal tubule in the rat, they affect different parts of that nephron segment. As with most nephrotoxicants, the mechanism(s) or subcellular target(s) for citrinin or chromate is unknown.
Citrinin mycotoxicosis in the rabbit.
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In three trials, single or multiple doses of citrinin dissolved in 0.5 N-NaOH and adjusted to neutral pH with HCl were given to rabbits by either the oral or intraperitoneal route. The 72-hr LD50 was 50 mg/kg body weight by intraperitoneal administration and 134 mg/kg by the oral route. The primary
Acute toxicity of citrinin in turkeys and ducklings.
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Citrinin, a naturally occurring mycotoxin, was dissolved in dimethyl-sulphoxide - 70% ethanol (3:1, v/v) and administered orally in two trials to 7-day-old male turkey poults and male white Pekin ducklings. The single dose LD50 value in 7-day-old male turkey poults was 56 mg/kg and in 7-day-old male
Mycotoxicoses produced in ducklings and turkeys by dietary and multiple doses of citrinin.
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Citrinin was mixed in the diet (100, 250, 500 parts/10(6)) and fed to 1-day-old male White Pekin ducklings (Trial I), or it was dissolved in dimethyl-sulphoxide-70% ethanol (3:1, v/v) and administered by crop gavage to 14-day-old male White Pekin ducklings (Trial II) or 7-day-old male turkey poults
Experimentally induced citrinin and endosulfan toxicity in pregnant Wistar rats: histopathological alterations in liver and kidneys of fetuses.
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In the present investigation, citrinin (CIT) (10 mg kg(-1) feed) and endosulfan (1 mg kg(-1) body weight) were administered orally alone and in combination to pregnant Wistar rats from gestational day 6 to 20 and their fetuses were collected to evaluate the histopathological alterations in hepatic
A potential role of calcium in apoptosis and aberrant chromatin forms in porcine kidney PK15 cells induced by individual and combined ochratoxin A and citrinin.
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The aim of this study was to establish the involvement of calcium signalling in genotoxicity, apoptosis and necrosis evoked by ochratoxin A (OTA) and citrinin (CTN) alone or in combination in porcine kidney PK15 cells. Cell proliferation test (MTT) and trypan blue assays (24 h) demonstrated that CTN
Ochratoxin A and citrinin induced nephrosis in Beagle dogs. II. Pathology.
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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
Evaluation of the developmental toxicity of citrinin using Hydra attenuata and postimplantation rat whole embryo culture.
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Citrinin (a mycotoxin produced as a frequent contaminant of food and feed by numerous species of Aspergillus and Penicillium fungi) is embryo/fetotoxic and embryocidal in mice and rats. The present study was designed to examine whether the in vivo observed developmental toxicity of citrinin could be
Citrinin mycotoxicosis in the rabbit: clinicopathological alterations.
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Citrinin, a nephrotoxic mycotoxin, was dissolved in 0.5 N-NaOH neutralized with HCl and given in a single oral dose of 120 mg/kg (Trial I) or 80 or 100 mg/kg (Trial II) to male New Zealand white rabbits weighing 2.0-2.7 kg. In Trial I, sequential measurements of clinicopathological parameters were
Studies on the sequential development and pathogenesis of citrinin mycotoxicosis in turkeys and ducklings.
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The toxic effects of citrinin in turkeys and ducklings was studied in four trials. Citrinin dissolved in dimethyl sulfoxide-70% ethanol solution (3:1, volume/volume) was administered by gavage to male turkey poults and male white Pekin ducklings. When seven-day-old ducklings were given doses of
Combined cell wall polysaccharide, mycotoxin and bacterial lipopolysaccharide exposure and inflammatory cytokine responses.
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Human exposure to environmental microbes occurs regularly. Microbial compounds may interact with each other to affect cellular responses. We hypothesized that interactions between microbial compounds could modulate inflammatory cytokine responses in vitro. We investigated monocyte production of the
Multiplexed assay panel of cytotoxicity in HK-2 cells for detection of renal proximal tubule injury potential of compounds.
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Proximal tubules of the kidneys are one of the most common targets of nephrotoxic drugs and chemicals. Screens to predict nephrotoxic potential of compounds with insights to mechanisms of toxicity facilitate lead optimization, guide structure-activity relationships, minimize risks of clinical
Structural and ultrastructural alterations in BALB/c mice: effects of Penicillium citrinum metabolites.
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The aims of this work were to determine the effect of feeding BALB/c mice a diet containing culture materials of a citrinin producing strain of Penicillium citrinum (Thom). Changes in hematological parameters, serum chemistry and histological changes in liver, kidney and heart were determined. After
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