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Effect of dietary manganese and vitamin E deficiencies on tissue antioxidant status in STZ-diabetic rats Thompson, Katherine Hirsch
Abstract
Interactions between manganese (Mn) deficiency and streptozotocin (STZ)-diabetes with respect to tissue antioxidant status were investigated in male, Sprague-Dawley rats. All rats were fed either a Mn-deficient (1 ppm) or a Mn-sufficient (45 ppm) diet for 8 weeks. Diabetes was then induced by tail-vein injection of STZ (60 mg/kg body weight), after which the rats were kept for an additional 4 to 8 weeks. The control groups comprised rats not injected with STZ, which were either Mn-deficient or Mn-sufficient. The Mn-deficient diet decreased the activities of manganese superoxide dismutase (MnSOD) in kidney and heart, and of copper-zinc superoxide dismutase (CuZnSOD) in kidney, in non-diabetic animals. In the diabetic rats, the Mn-deficient diet induced more pronounced decreases in activities of these same enzymes, and also increased liver MnSOD activity. Pancreas weights were significantly lower in Mn-deficient, compared to Mn-sufficient rats. Also, Mn-deficient, diabetic rats were significantly more hyperglycemic in response to a glucose load than Mn-sufficient, suggesting that they may have been more severely diabetic. Surprisingly, plasma and hepatic vitamin E levels increased progressively with the duration of diabetes. Lipid peroxidation, as measured by H₂O₂ -induced production of thiobarbituric acid reactive substances in erythrocytes, plasma lipoperoxides, and renal adipose tissue fluorescence, also increased concomitant with decreased liver and kidney glutathione levels. The effect of vitamin E-deficiency on Mn-deficient, diabetic rats was also investigated. Predictably, vitamin E-deficient rats were almost entirely depleted of plasma and liver vitamin E after 12 weeks on the deficient diets (4 weeks after STZ treatment). Consistent with this, tissue lipid peroxides were elevated compared to vitamin E-sufficient rats. Superimposing vitamin E-deficiency on manganese deficiency failed to add any further deficits in tissue antioxidant status. Higher glycosylated hemoglobin levels were observed in vitamin E-deficient, compared to vitamin E-sufficient, diabetic rats. These findings demonstrate for the first time an interactive effect between manganese deficiency and STZ-diabetes resulting in amplification of tissue antioxidant changes seen with either manganese deficiency or STZ-diabetes alone. This effect of cofactor deprivation in experimental diabetes raises the question of adequacy of the nominally Mn-sufficient diet in insulin-dependent diabetes mellitus.
Item Metadata
Title |
Effect of dietary manganese and vitamin E deficiencies on tissue antioxidant status in STZ-diabetic rats
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Creator | |
Publisher |
University of British Columbia
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Date Issued |
1991
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Description |
Interactions between manganese (Mn) deficiency and streptozotocin (STZ)-diabetes with respect to tissue antioxidant status were investigated in male, Sprague-Dawley rats. All rats were fed either a Mn-deficient (1 ppm) or a Mn-sufficient (45 ppm) diet for 8 weeks. Diabetes was then induced by tail-vein injection of STZ (60 mg/kg body weight), after which the rats were kept for an additional 4 to 8 weeks. The control groups comprised rats not injected with STZ, which were either Mn-deficient or Mn-sufficient.
The Mn-deficient diet decreased the activities of manganese superoxide dismutase (MnSOD) in kidney and heart, and of copper-zinc superoxide dismutase (CuZnSOD) in kidney, in non-diabetic animals. In the diabetic rats, the Mn-deficient diet induced more pronounced decreases in activities of these same enzymes, and also increased liver MnSOD activity. Pancreas weights were significantly lower in Mn-deficient, compared to Mn-sufficient rats. Also, Mn-deficient, diabetic rats were significantly more hyperglycemic in response to a glucose load than Mn-sufficient, suggesting that they may have been more severely diabetic.
Surprisingly, plasma and hepatic vitamin E levels increased progressively with the duration of diabetes. Lipid peroxidation, as measured by H₂O₂ -induced production of thiobarbituric acid reactive substances in erythrocytes, plasma
lipoperoxides, and renal adipose tissue fluorescence, also increased concomitant with decreased liver and kidney glutathione levels.
The effect of vitamin E-deficiency on Mn-deficient, diabetic rats was also investigated. Predictably, vitamin E-deficient rats were almost entirely depleted of plasma and liver vitamin E after 12 weeks on the deficient diets (4 weeks after STZ treatment). Consistent with this, tissue lipid peroxides were elevated compared to vitamin E-sufficient rats. Superimposing vitamin E-deficiency on manganese deficiency failed to add any further deficits in tissue antioxidant status. Higher glycosylated hemoglobin levels were observed in vitamin E-deficient, compared to vitamin E-sufficient, diabetic rats.
These findings demonstrate for the first time an interactive effect between manganese deficiency and STZ-diabetes resulting in amplification of tissue antioxidant changes seen with either manganese deficiency or STZ-diabetes alone. This effect of cofactor deprivation in experimental diabetes raises the question of adequacy of the nominally Mn-sufficient diet in insulin-dependent diabetes mellitus.
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Genre | |
Type | |
Language |
eng
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Date Available |
2011-03-09
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Provider |
Vancouver : University of British Columbia Library
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Rights |
For non-commercial purposes only, such as research, private study and education. Additional conditions apply, see Terms of Use https://open.library.ubc.ca/terms_of_use.
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DOI |
10.14288/1.0101143
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URI | |
Degree | |
Program | |
Affiliation | |
Degree Grantor |
University of British Columbia
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Campus | |
Scholarly Level |
Graduate
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Aggregated Source Repository |
DSpace
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For non-commercial purposes only, such as research, private study and education. Additional conditions apply, see Terms of Use https://open.library.ubc.ca/terms_of_use.