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Selenium alleviates porcine nephrotoxicity of ochratoxin A by improving selenoenzyme expression in vitro.

Gan F, Xue H, Huang Y, Pan C, Huang K - PLoS ONE (2015)

Bottom Line: Furthermore, selenomethionine enhanced the activity and mRNA and protein expression of glutathione peroxidase 1 (GPx1), mRNA expression of GPx4, and mRNA expression of thioredoxin reductase 1 in the presence and absence of OTA.Among them, promoting effect of selenomethionine on GPx1 was maximal.Therefore, selenomethionine supplementation may be an attractive strategy for protecting humans and animals from the risk of kidney damage induced by OTA.

View Article: PubMed Central - PubMed

Affiliation: College of Veterinary Medicine, Nanjing Agricultural University, Nanjing, Jiangsu Province, China.

ABSTRACT
Ochratoxin A (OTA), a mycotoxin, is a potent nephrotoxin in humans and animals. Selenium (Se) is an essential micronutrient for humans and animals, and plays a key role in antioxidant defense. To date, little is known about the effect of Se on OTA-induced nephrotoxicity. In this study, the protective effects of selenomethionine against OTA-induced nephrotoxicity were investigated using the porcine kidney 15 (PK15) cells as a model. The results showed that OTA induced nephrotoxicity in a dose-dependent manner. Se at 0.5, 1, 2 and 4 μM had significant protective effects against OTA-induced nephrotoxicity. Furthermore, selenomethionine enhanced the activity and mRNA and protein expression of glutathione peroxidase 1 (GPx1), mRNA expression of GPx4, and mRNA expression of thioredoxin reductase 1 in the presence and absence of OTA. Among them, promoting effect of selenomethionine on GPx1 was maximal. Knock-down of GPx1 by using a GPx1-specific siRNA eliminated the protective effects of selenomethionine against OTA-induced nephrotoxicity. The results suggest that selenomethionine alleviates OTA-induced nephrotoxicity by improving selenoenzyme expression in PK15 cells. Therefore, selenomethionine supplementation may be an attractive strategy for protecting humans and animals from the risk of kidney damage induced by OTA.

No MeSH data available.


Related in: MedlinePlus

Protective effects of selenomethionine against OTA-induced apoptosis in PK15 cells.Caspase-3 activity (A) and annexin V-binding (B) were assayed as described in the Materials and Methods section. Data are presented as mean ± SE (n = 3). Significance compared with control (without OTA or selenomethionine), *P < 0.05 and **P < 0.01. Within the OTA treatment group, significance compared with the control cells without selenomethionine treatment, #P < 0.05 and ##P < 0.01.
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pone.0119808.g003: Protective effects of selenomethionine against OTA-induced apoptosis in PK15 cells.Caspase-3 activity (A) and annexin V-binding (B) were assayed as described in the Materials and Methods section. Data are presented as mean ± SE (n = 3). Significance compared with control (without OTA or selenomethionine), *P < 0.05 and **P < 0.01. Within the OTA treatment group, significance compared with the control cells without selenomethionine treatment, #P < 0.05 and ##P < 0.01.

Mentions: To evaluate the protective effects of selenomethionine against OTA-induced apoptosis, PK15 cells were cultured with 0, 0.5, 1, 2, or 4 μM of Se (from selenomethionine) for 24 h and then incubated in the presence or absence of 2.5 μg/mL of OTA and Se for an additional 48 h. As shown in Fig. 3, OTA increased caspase-3 activity (Fig. 3A) and annexin V-binding in PK15 cells (Fig. 3B) (P < 0.05). Compared with OTA treatment controls, selenomethionine significantly reversed these OTA-induced changes in a dose dependent manner (P < 0.05). These results suggested that selenomethionine offered significant protection from OTA-induced apoptosis.


Selenium alleviates porcine nephrotoxicity of ochratoxin A by improving selenoenzyme expression in vitro.

Gan F, Xue H, Huang Y, Pan C, Huang K - PLoS ONE (2015)

Protective effects of selenomethionine against OTA-induced apoptosis in PK15 cells.Caspase-3 activity (A) and annexin V-binding (B) were assayed as described in the Materials and Methods section. Data are presented as mean ± SE (n = 3). Significance compared with control (without OTA or selenomethionine), *P < 0.05 and **P < 0.01. Within the OTA treatment group, significance compared with the control cells without selenomethionine treatment, #P < 0.05 and ##P < 0.01.
© Copyright Policy
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4372527&req=5

pone.0119808.g003: Protective effects of selenomethionine against OTA-induced apoptosis in PK15 cells.Caspase-3 activity (A) and annexin V-binding (B) were assayed as described in the Materials and Methods section. Data are presented as mean ± SE (n = 3). Significance compared with control (without OTA or selenomethionine), *P < 0.05 and **P < 0.01. Within the OTA treatment group, significance compared with the control cells without selenomethionine treatment, #P < 0.05 and ##P < 0.01.
Mentions: To evaluate the protective effects of selenomethionine against OTA-induced apoptosis, PK15 cells were cultured with 0, 0.5, 1, 2, or 4 μM of Se (from selenomethionine) for 24 h and then incubated in the presence or absence of 2.5 μg/mL of OTA and Se for an additional 48 h. As shown in Fig. 3, OTA increased caspase-3 activity (Fig. 3A) and annexin V-binding in PK15 cells (Fig. 3B) (P < 0.05). Compared with OTA treatment controls, selenomethionine significantly reversed these OTA-induced changes in a dose dependent manner (P < 0.05). These results suggested that selenomethionine offered significant protection from OTA-induced apoptosis.

Bottom Line: Furthermore, selenomethionine enhanced the activity and mRNA and protein expression of glutathione peroxidase 1 (GPx1), mRNA expression of GPx4, and mRNA expression of thioredoxin reductase 1 in the presence and absence of OTA.Among them, promoting effect of selenomethionine on GPx1 was maximal.Therefore, selenomethionine supplementation may be an attractive strategy for protecting humans and animals from the risk of kidney damage induced by OTA.

View Article: PubMed Central - PubMed

Affiliation: College of Veterinary Medicine, Nanjing Agricultural University, Nanjing, Jiangsu Province, China.

ABSTRACT
Ochratoxin A (OTA), a mycotoxin, is a potent nephrotoxin in humans and animals. Selenium (Se) is an essential micronutrient for humans and animals, and plays a key role in antioxidant defense. To date, little is known about the effect of Se on OTA-induced nephrotoxicity. In this study, the protective effects of selenomethionine against OTA-induced nephrotoxicity were investigated using the porcine kidney 15 (PK15) cells as a model. The results showed that OTA induced nephrotoxicity in a dose-dependent manner. Se at 0.5, 1, 2 and 4 μM had significant protective effects against OTA-induced nephrotoxicity. Furthermore, selenomethionine enhanced the activity and mRNA and protein expression of glutathione peroxidase 1 (GPx1), mRNA expression of GPx4, and mRNA expression of thioredoxin reductase 1 in the presence and absence of OTA. Among them, promoting effect of selenomethionine on GPx1 was maximal. Knock-down of GPx1 by using a GPx1-specific siRNA eliminated the protective effects of selenomethionine against OTA-induced nephrotoxicity. The results suggest that selenomethionine alleviates OTA-induced nephrotoxicity by improving selenoenzyme expression in PK15 cells. Therefore, selenomethionine supplementation may be an attractive strategy for protecting humans and animals from the risk of kidney damage induced by OTA.

No MeSH data available.


Related in: MedlinePlus