Carbon-14-Ochratoxin a Distribution in the Japanese Quail (Coturnix coturnix japonica) Monitored by Whole Body Autoradiography

Fuchs, Radovan; Appelgren, Lars‐Erik; Hagelberg, Sigrid; Hult, Karl

doi:10.3382/ps.0670707

Cited by 16 publications

(8 citation statements)

References 14 publications

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“…A significant increase in relative kidney and liver weights in OTA treated birds as observed in this study has also been reported by different scientists (Santin et al, 2002;Elaroussi et al, 2006). As liver and kidney are the primary organs being involved in the elimination of toxic materials from the body so the increased sizes of these organs might occur due to the damages caused during the elimination of OTA from the body through kidney and liver (Fuchs et al, 1988). Feeding bentonite clay did not cause any amelioration in OTA induced alterations in relative liver and kidney weights.…”

Section: Discussionsupporting

confidence: 88%

Toxicopathological and Serum Biochemical Alterations Induced by Ochratoxin a in Broiler Chicks and Their Amelioration by Locally Available Bentonite Clay

Khatoon¹,

Khan²,

Khan

et al. 2016

PAKJAS

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Ochratoxin A (OTA), a potent carcinogen, poses a great threat to the lives of poultry, animals and humans. It causes nephrotoxicity, immunosuppression, mutagenicity and teratogenicity in birds. Bentonite clay, belonging to the subclass of aluminosilicates, has the ability to adsorb different molecules and can efficiently adsorb several mycotoxins too. The present study was designed to evaluate the ameliorative effects of locally available bentonite clay against OTA induced toxicopathological and serum biochemical alterations in broilers. For this, day old broilers were divided into 16 equal groups and were given different combinations of OTA (0.15, 0.3 and 1.0 mg/kg feed) and bentonite clay (5, 10 and 20 g/kg feed). Results indicated that feeding OTA alone caused a reduction in body weight gain, poor FCR, increased gross lesions, altered relative organ weights and serum biochemical values and all these changes occurred in a dose dependent manner. Feeding bentonite clay along with OTA did not ameliorate the OTA induced alterations in body weight, FCR, gross lesions, relative organ weights and serum biochemical parameters.

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Section: Discussionsupporting

confidence: 88%

Toxicopathological and Serum Biochemical Alterations Induced by Ochratoxin a in Broiler Chicks and Their Amelioration by Locally Available Bentonite Clay

Khatoon¹,

Khan²,

Khan

et al. 2016

PAKJAS

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“…Following the acute administration of toxin to Wistar rats, the highest concentrations were measured in the papilla and inner medulla. However, during the chronic toxin exposure of adult rats, OTA concentrations were significantly higher in the cortex and external medulla (Kane et al 1986;Fuchs et al 1988;Schwerdt et al 1996).…”

Section: Discussionmentioning

confidence: 97%

Apoptosis and oxidative stress induced by ochratoxin A in rat kidney

et al. 2003

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Ochratoxin A (OTA) is a widespread mycotoxin produced by several species of fungi. OTA induces a tubular-interstitial nephropathy in humans and in animals. It has been implicated as one of the aetiological agents involved in the development of endemic nephropathy. OTA-induced oxidative stress and apoptosis may play key roles in the development of chronic tubulointerstitial nephritis connected to the long-term exposure to this food contaminant. We studied the effects of low doses of OTA on kidney cells. Wistar rats were treated with 120 microg OTA/kg bodyweight daily, for 10, 30 or 60 days. Toxin concentration in kidney was proportional to the time of exposure, and amounted to 547.2, 752.5 and 930.3 ng OTA/g kidney tissue after 10, 30 and 60 days, respectively. OTA treatment caused an increased number of cells undergoing apoptosis in both proximal and distal epithelial kidney cells. The apoptotic cells were visualised using the TUNEL assay and staining with haematoxylin and eosin in situ. The number of apoptotic cells in rats treated for 10, 30 and 60 days increased by 5-, 6.4- and 12.7-fold, respectively, compared with the control cells. However, DNA electrophoresis did not show characteristic fragmentation (DNA laddering). The oxidative stress was evident via increased malondialdehyde formation. The concentration of lipid peroxides showed an increase (36%), but the activity of superoxide dismutase decreased (26%) in 60-day treated rats. In spite of the observed biochemical and morphological changes in the kidney cells, renal functional status was preserved to the end of experiment. This study demonstrates that a combination of morphologic and biochemical markers can be used to monitor early cell death in OTA-induced renal injury. We have shown that the exposure to the relatively low OTA concentrations has activated apoptotic processes and oxidative damage in kidney cells.

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“…Besides its hepatotoxic, immunosuppreseant, teratogenic, neurotoxic, and mutagenic effects (Zahoor-ul-Hassan et al 2010;Wangikar et al 2007;Elaroussi et al 2006;Sava et al 2006;Kumar et al 2004;Gilani, Bancroft, and Reily 1978), it has also been classified by the International Agency for Research on Cancer (IARC; 1993) as a possible human carcinogen (2B). In experimental studies, residues of OTA have been detected in the blood and tissues (Denli et al 2008;Biro et al 2002;Niemiec et al 1994) and also in the eggs (Frye and Chu 1978;Fuchs et al 1988;Niemiec et al 1994) of birds kept on OTAcontaminated ration. Teratogenic and embryotoxic effects of OTA alone and in combination with other mycotoxins have been reported in rat, rabbit, and chicken (Wangikar et al 2007(Wangikar et al , 2005Wangikar, Dwivedi, and Sinha 2004;Wei and Sulik 1996;Vesala, Vesely, and Jelinek 1983;Gilani, Bancroft, and Reily 1978).…”

Section: Introductionmentioning

confidence: 99%

Toxico-Pathological Effects of In Ovo Inoculation of Ochratoxin A (OTA) in Chick Embryos and Subsequently in Hatched Chicks

et al. 2011

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This study was designed to investigate the toxico-pathological effects of in ovo inoculation of ochratoxin A (OTA) in chicken embryos and subsequently in the hatching chicks. Nine hundred fertile white leghorn (WL) layer breeder eggs were divided into eight groups (A-H). Group A was maintained as untreated control, whereas group B was kept as sham control (10 mL of 0.1 M NaHCO 3 solution). Before incubation, groups C, D, E, F, G, and H were injected with 0.01, 0.03, 0.05, 0.10, 0.50, and 1.00 mg OTA/egg, respectively. At 53 hrs of incubation, crown to rump length, optic cups, and eye lens diameters were significantly (p .05) lower, whereas neural tube closure defects were higher in the OTA-treated embryos. Teratogenic defects (studied at day 9 of incubation) and embryonic mortalities were higher in the groups administered high doses of OTA. A significant increase was noted in the serum concentration of ALT, urea, and creatinine, along with higher weights of liver and kidney, in chicks hatched from OTA-contaminated eggs. These findings suggested that there are teratogenic and substantive toxicological risks in the developing chicken embryos and hatched chicks that could be exposed to OTA in ovo.

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Carbon-14-Ochratoxin a Distribution in the Japanese Quail (Coturnix coturnix japonica) Monitored by Whole Body Autoradiography

Cited by 16 publications

References 14 publications

Toxicopathological and Serum Biochemical Alterations Induced by Ochratoxin a in Broiler Chicks and Their Amelioration by Locally Available Bentonite Clay

Toxicopathological and Serum Biochemical Alterations Induced by Ochratoxin a in Broiler Chicks and Their Amelioration by Locally Available Bentonite Clay

Apoptosis and oxidative stress induced by ochratoxin A in rat kidney

Toxico-Pathological Effects of In Ovo Inoculation of Ochratoxin A (OTA) in Chick Embryos and Subsequently in Hatched Chicks

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