Effects of Single and Repeated Oral Doses of Ochratoxin A on the Lipid Peroxidation and Antioxidant Defense Systems in Mouse Kidneys

doi:10.3390/toxins12110732

. 2020 Nov 22;12(11):732.

doi: 10.3390/toxins12110732.

Effects of Single and Repeated Oral Doses of Ochratoxin A on the Lipid Peroxidation and Antioxidant Defense Systems in Mouse Kidneys

Affiliations

¹ Institute of Experimental Medicine, Laboratory of Molecular Neuroendocrinology, 43. Szigony Street, Budapest 1083, Hungary.
² Szent István University, Department of Environmental Protection & Safety, 1. Páter K. Street, Gödöllő 2100, Hungary.
³ Central Environmental and Food Science Research Institute, Department of Microbiology, 15. Herman O. Street, Budapest 1022, Hungary.
⁴ National Agricultural Research and Innovation Center, Agricultural Biotechnology Institute, Reproduction Biology and Toxicology Research Group, 4. Szent-Györgyi A. Street, Gödöllő 2100, Hungary.
⁵ CEVA Phylaxia Ltd, 5. Szállás Street, Budapest 1107, Hungary.
⁶ Szent István University, Department of Nutrition, 1. Páter K. Street, Gödöllő 2100, Hungary.
⁷ "MTA-KE-SZIE Mycotoxins in the Food Chain" Research Group, Hungarian Academy of Science, Kaposvár University, 40. Guba Sándor Street, Kaposvár 7400, Hungary.

PMID: 33266415
PMCID: PMC7700583
DOI: 10.3390/toxins12110732

Free PMC article

Effects of Single and Repeated Oral Doses of Ochratoxin A on the Lipid Peroxidation and Antioxidant Defense Systems in Mouse Kidneys

Szilamér Ferenczi et al. Toxins (Basel). 2020.

Free PMC article

. 2020 Nov 22;12(11):732.

doi: 10.3390/toxins12110732.

Authors

Affiliations

¹ Institute of Experimental Medicine, Laboratory of Molecular Neuroendocrinology, 43. Szigony Street, Budapest 1083, Hungary.
² Szent István University, Department of Environmental Protection & Safety, 1. Páter K. Street, Gödöllő 2100, Hungary.
³ Central Environmental and Food Science Research Institute, Department of Microbiology, 15. Herman O. Street, Budapest 1022, Hungary.
⁴ National Agricultural Research and Innovation Center, Agricultural Biotechnology Institute, Reproduction Biology and Toxicology Research Group, 4. Szent-Györgyi A. Street, Gödöllő 2100, Hungary.
⁵ CEVA Phylaxia Ltd, 5. Szállás Street, Budapest 1107, Hungary.
⁶ Szent István University, Department of Nutrition, 1. Páter K. Street, Gödöllő 2100, Hungary.
⁷ "MTA-KE-SZIE Mycotoxins in the Food Chain" Research Group, Hungarian Academy of Science, Kaposvár University, 40. Guba Sándor Street, Kaposvár 7400, Hungary.

PMID: 33266415
PMCID: PMC7700583
DOI: 10.3390/toxins12110732

Abstract

Ochratoxin-A (OTA) is a carcinogenic and nephrotoxic mycotoxin, which may cause health problems in humans and animals, and it is a contaminant in foods and feeds. The purpose of the present study is to evaluate the effect of oral OTA exposure on the antioxidant defense and lipid peroxidation in the kidney. In vivo administration of OTA in CD1, male mice (1 or 10 mg/kg body weight in a single oral dose for 24 h and repeated daily oral dose for 72 h or repeated daily oral dose of 0.5 mg/kg bodyweight for 21 days) resulted in a significant elevation of OTA levels in blood plasma. Some histopathological alterations, transcriptional changes in the glutathione system, and oxidative stress response-related genes were also found. In the renal cortex, the activity of the glutathione-system-related enzymes and certain metabolites of the lipid peroxidation (conjugated dienes, trienes, and thiobarbituric reactive substances) also changed.

Keywords: gene expression; glutathione; kidney; ochratoxin-A; oxidative stress.

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Conflict of interest statement

The authors declare no conflict of interest.

Figures

**Figure 1**
Effect of OTA expositions on GPx activity in the kidney cortex. (A) GPx activity of kidney samples in case of single oral dose (24 h) OTA treatment. The applied OTA doses did not change significantly the GPx activity. (B) GPx activity of kidney samples in case of repeated daily oral dose (72 h) OTA treatment. The highest applied OTA dose decreased significantly (p < 0.05) the GPx activity. (C) GPx activity of kidney samples in case of repeated daily oral dose (21 days) OTA treatment. The applied OTA dose did not change the GPx activity significantly. Abbreviations: MMS: methyl-methanesulfonate-treated group; OTA 1 and OTA 10: treatment with 1 and 10 mg/kg bw ochratoxin A in the single oral dose (24 h) and repeated daily oral dose (72 h); OTA 0.5: 0.5 mg/kg bw ochratoxin A treatment in the repeated daily oral dose (21 days) experiment. Mean ± S.D. Data were analyzed by one-way ANOVA and Tukey’s post hoc test.* p < 0.05 vs. vehicle.

**Figure 2**
Effect of OTA expositions on the glutathione reductase (GR) activity in the kidney cortex. (A) GR activity of kidney samples in case of single oral dose (24 h) OTA treatment. The applied OTA doses did not change significantly the GR activity. (B) GR activity of kidney samples in case of repeated daily oral dose (72 h) OTA treatment. The applied OTA doses did not change significantly the GR activity. (C) GR activity of kidney samples in case of repeated daily oral dose (21 days) OTA treatment. The applied OTA dose did not change the GR activity significantly. Abbreviations: MMS: methyl-methanesulfonate-treatment group; OTA 1 and OTA 10: 1 and 10 mg/kg bw ochratoxin A treatment in the single oral dose (24 h) and repeated daily oral dose (72 h) groups; OTA 0.5: 0.5 mg/kg bw ochratoxin A treatment in the repeated daily oral dose (21 days) group. Mean ± S.D. Data were analyzed by one-way ANOVA and Tukey’s post hoc test. * p < 0.05 vs. vehicle.

**Figure 3**
Effect of single oral dose (24 h) OTA exposure on lipid peroxidation parameters and reduced and oxidized glutathione concentration in the kidney cortex. (A) Levels of conjugated dienes (CD) in kidney samples in case of single oral dose (24 h) OTA treatment. The applied OTA doses did not cause significant alterations. (B) Levels of conjugated trienes (CT) in kidney samples in case of single oral dose (24 h) OTA treatment. The applied OTA doses did not cause significant alteration. (C) Malondialdehyde (MDA) concentration in kidney samples in case of single oral dose (24 h) OTA treatment. The applied OTA doses did not cause significant changes. (D) Reduced glutathione (GSH) concentration in kidney samples in case of single oral dose (24 h) OTA treatment. Both applied OTA doses decreased significantly (p < 0.01) the GSH concentration. (E) Oxidized glutathione (GSSG) concentration in kidney samples in case of single oral dose (24 h) OTA treatment. Both applied OTA doses decreased (p < 0.01 and p < 0.05, respectively) the GSSG concentration significantly. Abbreviations: MMS: methyl-methanesulfonate-treatment. OTA 1 and OTA 10: 1 and 10 mg/kg bw ochratoxin A-treated groups. Mean ± S.D. Data were analyzed by one-way ANOVA and Tukey’s post hoc test. * p < 0.05, ** p < 0.01 vs. vehicle.

**Figure 4**
The effect of repeated daily oral dose (72 h) OTA exposition on some lipid peroxidation parameters and reduced and oxidized glutathione concentration in the kidney cortex. A: Levels of conjugated dienes (CD) in kidney samples in case of repeated daily oral dose (72 h) OTA treatment. The highest OTA dose increased significantly (p < 0.01) the level of conjugated dienes in the kidney. B: Levels of conjugated trienes (CT) in kidney samples in case of repeated daily oral dose (72 h) OTA treatment. The applied OTA doses did not cause significant alterations. C: Malondialdehyde (MDA) concentration in kidney samples in case of repeated daily oral dose (72 h) OTA treatment. The applied OTA doses did not cause significant changes. D: Reduced glutathione (GSH) concentration in kidney samples in case of repeated daily oral dose (72 h) OTA treatment. The applied OTA doses did not cause significant alterations. E: Oxidized glutathione (GSSG) concentration in kidney samples in case of repeated daily oral dose (72 h) OTA treatment. The applied OTA doses did not significantly alter, while the MMS treatment increased the GSSG concentration significantly (p < 0.01). Abbreviations: MMS: methyl-methanesulfonate-treated group; OTA 1 and OTA 10: 1 and 10 mg/kg bw ochratoxin-A-treated groups. Mean ± S.D. Data were analyzed by one-way ANOVA and Tukey’s post hoc test. ** p < 0.01 vs. vehicle.

**Figure 5**
Effect of repeated daily oral dose (21 days) OTA exposition on lipid peroxidation parameters and reduced and oxidized glutathione concentration in the kidney cortex. A: Levels of conjugated dienes (CD) in kidney samples in case of repeated daily oral dose (21 days) OTA treatment. The applied OTA dose did not cause significant alteration. B: Levels of conjugated trienes (CT) in kidney samples in case of repeated daily oral dose (21 days) OTA treatment. The applied OTA dose did not cause significant alteration. C: Malondialdehyde (MDA) concentration in kidney samples in case of repeated daily oral dose (21 days) (21 days) OTA treatment. The applied OTA dose increased the MDA concentration in the kidney significantly (*** p < 0.001). D: Reduced glutathione (GSH) concentration in kidney samples in case of repeated daily oral dose (21 days) OTA treatment. The applied OTA dose decreased significantly (* p < 0.05), the GSH concentration in the kidney. E: Oxidized glutathione (GSSG) concentration in the case of kidney samples in repeated daily oral dose (21 days) OTA treatment. The MMS treatment and the applied OTA dose increased significantly (*** p < 0.001 and * p < 0.05, respectively) the GSSG concentration in the kidney. Abbreviations: MMS: methyl-methanesulfonate-treated group; OTA 0.5: 0.5 mg/kg bw ochratoxin-A-treated group. Mean ± S.D. Data were analyzed by one-way ANOVA and Tukey’s post hoc test. * p < 0.05, *** p < 0.001 vs. vehicle.

**Figure 6**
Effect of OTA expositions on the *Gsta* gene expression in the kidney cortex. A: *Gsta* gene expression alterations of the single oral dose (24 h) OTA-treated kidney samples. The highest OTA dose decreased the *Gsta* mRNA level (p < 0.01). B: *Gsta* gene expression alterations of the repeated daily oral dose (72 h) OTA-treated kidney samples. Both applied OTA doses decreased the *Gsta* mRNA levels (p < 0.01). C: *Gsta* gene expression alterations of the repeated daily oral dose (21 days) OTA-treated kidney samples. OTA treatment did not influence the *Gsta* mRNA level. Abbreviations: MMS: methyl-methanesulfonate-treated group; OTA 1 and OTA 10: 1 and 10 mg/kg bw ochratoxin-A-treated groups in the single oral dose (24 h) and repeated daily oral dose (72 h) experiment; OTA 0.5: 0.5 mg/kg bw ochratoxin-A-treated group in the repeated daily oral dose (21 days) experiment. Mean ± S.D. Data were analyzed by one-way ANOVA and Tukey’s post hoc test. * p < 0.05, ** p < 0.01, *** p < 0.001 vs. vehicle.

**Figure 7**
Effect of OTA expositions on the *Gpx1* and *Gpx2* mRNA expression levels in the kidney cortex. A: *Gpx1* gene mRNA expressions of the single oral dose (24 h) OTA-treated kidney samples. OTA treatment did not influence the *Gpx1* mRNA level. B: *Gpx1* gene expression levels of the repeated daily oral dose (72 h) OTA-treated kidney samples. Both applied OTA doses decreased the *Gpx1* mRNA levels (p < 0.001). C: *Gpx1* gene expression alterations of the repeated daily oral dose (21 days) OTA-treated kidney samples. The applied OTA dose decreased the *Gpx1* mRNA level (p < 0.01). D: *Gpx2* gene expression of the single oral dose (24 h) OTA-treated kidney samples. Both applied OTA doses increased the *Gpx2* mRNA levels (p < 0.05). E: *Gpx2* gene expression alterations of the repeated daily oral dose (72 h) OTA-treated kidney samples. Both applied OTA doses decreased the *Gpx1* mRNA levels (p < 0.001). F: *Gpx2* gene expression levels of the repeated daily oral dose (21 days) OTA-treated kidney samples. OTA treatment did not significantly influence the *Gpx2* mRNA level. Abbreviations: MMS: methyl-methanesulfonate-treated group; OTA 1 and OTA 10: 1 and 10 mg/kg bw ochratoxin-A-treated groups in the single oral dose (24 h) and repeated daily oral dose (72 h) experiment; OTA 0.5: 0.5 mg/kg bw ochratoxin-A-treated group in the repeated daily oral dose (21 days) experiment. Mean ± S.D. Data were analyzed by one-way ANOVA and Tukey’s post hoc test. * p < 0.05, ** p < 0.01, **** p < 0.0001 vs. vehicle.

**Figure 8**
Effect of OTA expositions on the *Nrf2* mRNA expression levels in the kidney. (A) *Nrf2* gene mRNA expressions of the single oral dose (24 h) OTA-treated kidney samples. Both applied OTA doses increased the *Nrf2* mRNA levels (p < 0.01 and 0.0001, respectively). (B) *Nrf2* gene expression levels of the repeated daily oral dose (72 h) OTA-treated kidney samples. Both applied OTA doses increased the *Nrf2* mRNA levels (p < 0.01 and 0.0001, respectively). (C) *Nrf2* gene expression alterations of the repeated daily oral dose (21 days) OTA-treated kidney samples. The applied OTA dose increased the *Nrf2* mRNA level (** p < 0.01). Abbreviations: MMS: methyl-methanesulfonate-treated group; OTA 1 and OTA 10: 1 and 10 mg/kg bw ochratoxin-A-treated groups in the single oral dose (24 h) and repeated daily oral dose (72 h) experiment; OTA 0.5: 0.5 mg/kg bw ochratoxin-A-treated group in the repeated daily oral dose (21 days) experiment. Mean ± S.D. Data were analyzed by one-way ANOVA and Tukey’s post hoc test. ** p < 0.01, **** p < 0.0001 vs. vehicle.

**Figure 9**
Effect of single oral dose (24 h) OTA expositions on the NRF2 protein expression levels in the kidney. (A) Quantification of protein expression normalized to vehicle-treated controls by densitometry. Significant differences were found in the OTA-treated animals. (B) Representative examples of Western blots using kidney homogenates from mice. Abbreviations: MMS: methyl-methanesulfonate-treated group; OTA 1 and OTA 10: 1 and 10 mg/kg bw ochratoxin-A-treated groups in the single oral dose (24 h) experiment. Mean ± S.D. Data were analyzed by one-way ANOVA and Tukey’s post hoc test. * p < 0.05, ** p < 0.01 vs. vehicle.

**Figure 10**
Effect of repeated daily oral dose (72 h) OTA expositions on the expression of NRF2 protein in the kidney. (A) Protein expression normalized to vehicle-treated controls by densitometry. Significant protein expression elevation was found in the high dose of OTA-treated animals. (B) Representative examples of Western blots from kidney homogenates mice. Abbreviations: MMS: methyl-methanesulfonate-treated group; OTA 1 and OTA 10: 1 and 10 mg/kg bw ochratoxin-A-treated groups in the repeated daily oral dose (72 h) experiment. Mean ± S.D. Data were analyzed by one-way ANOVA and Tukey’s post hoc test. ** p < 0.01 vs. vehicle.

**Figure 11**
Effect of OTA expositions on the *Keap1* mRNA expression levels in the kidney. A: *Keap1* gene mRNA expressions of the single oral dose (24 h) OTA-treated kidney samples. The highest OTA dose decreased the *Keap1* mRNA level (p < 0.01). B: *Keap1* gene expression levels of the repeated daily oral dose (72 h) OTA-treated kidney samples. Both applied OTA doses decreased the *Keap1* mRNA levels (p < 0.05). C: *Keap1* gene expression alterations of the repeated daily oral dose (21 days) OTA-treated kidney samples. The OTA treatment did not influence the *Keap1* mRNA level significantly. Abbreviations: MMS: methyl-methanesulfonate-treated group, OTA 1; and OTA 10: 1 and 10 mg/kg bw ochratoxin-A-treated groups in the single oral dose (24 h) and repeated daily oral dose (72 h) experiment; OTA 0.5: 0.5 mg/kg bw ochratoxin-A-treated group in the repeated daily oral dose (21 days) experiment. Mean ± S.D. Data were analyzed by one-way ANOVA and Tukey’s post hoc test.* p < 0.05, ** p < 0.01 vs. vehicle.

**Figure 12**
Effect of OTA expositions on the hem-oxygenase (*Ho-1*) gene expression levels in the kidney. A: *Ho-1* gene mRNA expressions of the single oral dose (24 h) OTA-treated kidney samples. The OTA treatment had no significant effect on the *Ho-1* mRNA level. B: *Ho-1* gene expression levels of the repeated daily oral dose (72 h) OTA-treated kidney samples. The high dose of OTA treatment increased the *Ho-1* mRNA level significantly (p < 0.05). C: *Ho-1* gene expression alterations of the repeated daily oral dose (21 days) OTA-treated kidney samples. The OTA treatment did not influence significantly the *Ho-1* mRNA level. Abbreviations: MMS: Group treated with methyl-methanesulfonate; OTA 1 and OTA 10: groups treated with 1 and 10 mg/kg bw ochratoxin A in the single oral dose (24 h) and repeated daily oral dose (72 h) experiment; OTA 0.5: group treated with 0.5 mg/kg bw ochratoxin A in the repeated daily oral dose (21 days) experiment. Values are expressed as the mean ± SD. Data were analyzed by one-way ANOVA followed by Tukey’s post hoc test.* p < 0.05 vs. vehicle.

**Figure 13**
Effect of OTA expositions on the *Nqo1* mRNA expression levels in the kidney. A: *Nqo1* gene mRNA expressions of the single oral dose (24 h) OTA-treated kidney samples. Both applied OTA doses decreased the *Nqo1* mRNA levels (p < 0.01 and p < 0.001, respectively). B: *Nqo1* gene expression levels of the repeated daily oral dose (72 h) OTA-treated kidney samples. Both applied OTA doses decreased the *Nqo1* mRNA levels (p < 0.01, and p < 0.05, respectively). C: *Nqo1* gene expression alterations of the repeated daily oral dose (21 days) OTA-treated kidney samples. The OTA treatment did not have a significant effect on the *Nqo1* mRNA level. Abbreviations: MMS: methyl-methanesulfonate-treated treated group; OTA 1 and OTA 10: 1 and 10 mg/kg bw ochratoxin-A-treated groups in the single oral dose (24 h) and repeated daily oral dose (72 h) experiment; OTA 0.5: 0.5 mg/kg bw ochratoxin-A-treated group in the repeated daily oral dose (21 days) experiment. Mean ± S.D. Data were analyzed by one-way ANOVA and Tukey’s post hoc test.* p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001 vs. vehicle.

**Figure 14**
Effect of OTA expositions on the *Gss* mRNA expression levels in the kidney. A: *Gss* gene mRNA expressions of the single oral dose (24 h) OTA-treated kidney samples. The highest OTA dose decreased the *Gss* mRNA levels (p < 0.001). B: *Gss* gene expression levels of the repeated daily oral dose (72 h) OTA-treated kidney samples. The highest OTA dose decreased the *Gss* mRNA levels (p < 0.01). C: *Gss* gene expression alterations of the repeated daily oral dose (21 days) OTA-treated kidney samples. The applied OTA dose did not cause significant alteration. Abbreviations: MMS: methyl-methanesulfonate-treated group; OTA 1 and OTA 10: 1 and 10 mg/kg bw ochratoxin-A-treated groups in the single oral dose (24 h) and repeated daily oral dose (72 h) experiment; OTA 0.5: 0.5 mg/kg bw ochratoxin-A-treated group in the repeated daily oral dose (21 days) experiment. Mean ± S.D. Data were analyzed by one-way ANOVA and Tukey’s post hoc test. ** p < 0.01, *** p < 0.001 vs. vehicle.

**Figure 15**
Effect of OTA expositions on the *Sod1* and *Sod2* mRNA expression levels in the kidney. A: *Sod1* gene mRNA expressions of the single oral dose (24 h) OTA-treated kidney samples. The high OTA dose significantly increased the *Sod1* mRNA level (p < 0.05). B: *Sod1* gene expression levels of the repeated daily oral dose (72 h) OTA-treated kidney samples. Both OTA administration significantly decreased the *Sod1* mRNA level (p < 0.001 and 0.0001, respectively). C: *Sod1* gene expression alterations of the repeated daily oral dose (21 days) OTA-treated kidney samples. The OTA treatment did not significantly influence the *Sod1* mRNA level. D: *Sod2* gene mRNA expressions of the single oral dose (24 h) OTA-treated kidney samples. The OTA treatment did not significantly influence the *Sod2* mRNA level. E: *Sod2* gene expression levels of the repeated daily oral dose (72 h) OTA-treated kidney samples. The high OTA dose treatment significantly decreased the *Sod2* mRNA level (p < 0.001), F: *Sod2* gene expression alterations of the repeated daily oral dose (21 days) OTA-treated kidney samples. The OTA treatment did not significantly influence the *Sod2* mRNA level. Abbreviations: MMS: methyl-methanesulfonate-treated group; OTA 1 and OTA 10: 1 and 10 mg/kg bw ochratoxin-A-treated groups in the single oral dose (24 h) and repeated daily oral dose (72 h) experiment; OTA 0.5: 0.5 mg/kg bw ochratoxin-A-treated group in the repeated daily oral dose (21 days) experiment. Mean ± S.D. Data were analyzed by one-way ANOVA and Tukey’s post hoc test * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001 vs. vehicle.

**Figure 16**
Effect of OTA expositions on the *Hace1* and *Rac1* mRNA expression levels in the kidney. A: *Hace1* gene mRNA expressions of the single oral dose (24 h) OTA-treated kidney samples. The high OTA dose significantly increased the *Hace1* mRNA level (p < 0.01). B: *Hace1* gene expression levels of the repeated daily oral dose (72 h) OTA-treated kidney samples. Both OTA administrations significantly decreased the *Hace1* mRNA level (p < 0.0001). C: *Hace1* gene expression alterations of the repeated daily oral dose (21 days) OTA-treated kidney samples. The OTA treatment significantly increased the *Hace1* mRNA level (p < 0.05). D: *Rac1* gene mRNA expressions of the single oral dose (24 h) OTA-treated kidney samples. The OTA treatment did not significantly influence the *Rac1* mRNA level. E: *Rac1* gene expression levels of the repeated daily oral dose (72 h) OTA-treated kidney samples. The high OTA dose treatment significantly increased the *Rac1* mRNA level (p < 0.001), F: *Rac1* gene expression alterations of the repeated daily oral dose (21 days) OTA-treated kidney samples. The OTA treatment did not significantly influence the *Rac1* mRNA level. Abbreviations: MMS: methyl-methanesulfonate-treated group; OTA 1 and OTA 10: 1 and 10 mg/kg bw ochratoxin-A-treated groups in the single oral dose (24 h) and repeated daily oral dose (72 h) experiment; OTA 0.5: 0.5 mg/kg bw ochratoxin-A-treated group in the repeated daily oral dose (21 days) experiment. Mean ± S.D. Data were analyzed by one-way ANOVA and Tukey’s post hoc test.* p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001 vs. vehicle.

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References

1. Van Der Merwe K.J., Steyn P.S., Fourie L., Scott D.B., Theron J.J. Ochratoxin A, a Toxic Metabolite produced by Aspergillus ochraceus Wilh. Nat. Cell Biol. 1965;205:1112–1113. doi: 10.1038/2051112a0. - DOI - PubMed
1. Krogh P., Hald B., Pedersen E.J. Occurrence of Ochratoxin A and Citrinin in Cereals Associated with Mycotoxic Porcine Nephropathy. Acta Pathol. Microbiol. Scand. Sect. B Microbiol. Immunol. 1973;81:689–695. doi: 10.1111/j.1699-0463.1973.tb02261.x. - DOI - PubMed
1. Krogh P. Ochratoxin A residues in tissues of slaughter pigs with nephropathy. Nord. Veter. 1977;29:402–405. - PubMed
1. Elling F., Krogh P. Fungal Toxins and Balkan (Endemic) Nephropathy. Lancet. 1977;1:1213. doi: 10.1016/S0140-6736(77)92761-1. - DOI - PubMed
1. Krogh P., Hald B., Plestina R., Ceović S. Balkan (endemic) nephropathy and foodborn ochratoxin A: Preliminary results of a survey of foodstuffs. Acta Pathol. Microbiol. Scand. Sect. B Microbiol. 1977;85:238–240. doi: 10.1111/j.1699-0463.1977.tb01702.x. - DOI - PubMed

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[1] Van Der Merwe K.J., Steyn P.S., Fourie L., Scott D.B., Theron J.J. Ochratoxin A, a Toxic Metabolite produced by Aspergillus ochraceus Wilh. Nat. Cell Biol. 1965;205:1112–1113. doi: 10.1038/2051112a0. - DOI - PubMed

[2] Van Der Merwe K.J., Steyn P.S., Fourie L., Scott D.B., Theron J.J. Ochratoxin A, a Toxic Metabolite produced by Aspergillus ochraceus Wilh. Nat. Cell Biol. 1965;205:1112–1113. doi: 10.1038/2051112a0. - DOI - PubMed

[3] Krogh P., Hald B., Pedersen E.J. Occurrence of Ochratoxin A and Citrinin in Cereals Associated with Mycotoxic Porcine Nephropathy. Acta Pathol. Microbiol. Scand. Sect. B Microbiol. Immunol. 1973;81:689–695. doi: 10.1111/j.1699-0463.1973.tb02261.x. - DOI - PubMed

[4] Krogh P., Hald B., Pedersen E.J. Occurrence of Ochratoxin A and Citrinin in Cereals Associated with Mycotoxic Porcine Nephropathy. Acta Pathol. Microbiol. Scand. Sect. B Microbiol. Immunol. 1973;81:689–695. doi: 10.1111/j.1699-0463.1973.tb02261.x. - DOI - PubMed

[5] Krogh P. Ochratoxin A residues in tissues of slaughter pigs with nephropathy. Nord. Veter. 1977;29:402–405. - PubMed

[6] Krogh P. Ochratoxin A residues in tissues of slaughter pigs with nephropathy. Nord. Veter. 1977;29:402–405. - PubMed

[7] Elling F., Krogh P. Fungal Toxins and Balkan (Endemic) Nephropathy. Lancet. 1977;1:1213. doi: 10.1016/S0140-6736(77)92761-1. - DOI - PubMed

[8] Elling F., Krogh P. Fungal Toxins and Balkan (Endemic) Nephropathy. Lancet. 1977;1:1213. doi: 10.1016/S0140-6736(77)92761-1. - DOI - PubMed

[9] Krogh P., Hald B., Plestina R., Ceović S. Balkan (endemic) nephropathy and foodborn ochratoxin A: Preliminary results of a survey of foodstuffs. Acta Pathol. Microbiol. Scand. Sect. B Microbiol. 1977;85:238–240. doi: 10.1111/j.1699-0463.1977.tb01702.x. - DOI - PubMed

[10] Krogh P., Hald B., Plestina R., Ceović S. Balkan (endemic) nephropathy and foodborn ochratoxin A: Preliminary results of a survey of foodstuffs. Acta Pathol. Microbiol. Scand. Sect. B Microbiol. 1977;85:238–240. doi: 10.1111/j.1699-0463.1977.tb01702.x. - DOI - PubMed

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Effects of Single and Repeated Oral Doses of Ochratoxin A on the Lipid Peroxidation and Antioxidant Defense Systems in Mouse Kidneys

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Effects of Single and Repeated Oral Doses of Ochratoxin A on the Lipid Peroxidation and Antioxidant Defense Systems in Mouse Kidneys

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