Table 2 Antioxidant capacity against hydroxyl ORAC OH and peroxyl radical ORAC

Table 2 antioxidant capacity against hydroxyl orac oh

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Table 2. Antioxidant capacity against hydroxyl- ( ORAC -OH ) and peroxyl- radical (ORAC - ROO ) in different brain regions of the streptozotocin-induced diabetic (10 weeks) rats with or without manifested peripheral diabetic neuropathy. Region Treatment ORAC -OH ( µmol/g fresh tissue) ORAC- ROO ( µmol/g fresh tissue) CB C (4) 2474.6 1747.6 6261.7 2360.5 STZ-D (4) 2740.3 1705.0 3230.1 1595.0 * STZ+D (5) 1932.2 592.9 3156.8 383.7 * STZ+Dn (5) 1675.0 721.3 5605.9 1840.4 * BS C (4) 216.9 162.7 3637.0 826.6 STZ-D (4) 494.4 434.1 2866.0 1156.8 STZ+D (5) 360.4 201.7 3402.3 1136.8 STZ+Dn (5) 341.6 136.1 3376.6 443.5 Data are expressed as mean ± SD; number of animals is given in parenthesis. ORAC- oxygen radical absorbance capacity assay; CB- cerebellum; BS- brain stem; HPC- hippocampus; ND- no data; C- control group; STZ –D group treated parentherally with a diabetogenic streptozotocin dose which did not become diabetic; STZ+D streptozotocin-induced diabetic group which did not develop peripheral neuropathy; STZ+Dn streptozotocin-induced diabetic group which developed peripheral neuropathy. * p< 0.05 vs. control group by Student t-test. 9
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Table 3. Antioxidant capacity against hydroxyl- (ORAC -OH ) and peroxyl- radical (ORAC - ROO ) in different brain regions of the alloxan-induced diabetic (21 weeks) rats. I had to omit the line with data about AL rats which did not develop diabetes because it was only 1 animal. Region Treatment ORAC- OH (µmol/g fresh tissue) ORAC- ROO (µmol/g fresh tissue) CB C (4) 510.3 219.2 2061.3 182.0 AL+D (4) 432.4 206.3 *(a) 2117.7 265.3 BS C (3) 584.4 163.5 1737.4 268.4 AL+D (5) 435.3 164.2 *(b) 1479.9 129.9 * HPC C (4) 660.5 60.4 1906.2 212.3 AL+D (4) 595.3 61.8 *(c) 2066.7 347.0 Data are expressed as mean ± SD; number of animals is given in parenthesis. ORAC- oxygen radical absorbance capacity assay; CB- cerebellum; BS- brain stem; HPC- hippocampus; C-control group; AL+D alloxan-induced diabetic group; * p< 0.05 vs. control group by Student t-test. In comparison to the controls, significantly decreased AC against the hydroxyl-radical (ORAC- OH values) was found in the cerebellum and the brain stem of the STZ-icv treated rats while AC against the peroxyl-radical (ORAC- ROO values) remained unchanged (Table 4). In the TG-icv treated rats decrement of the AC was even more pronounced since significantly decreased ORAC- ROO levels were found in the hippocampus and significantly decreased ORAC- OH levels were fund in all three investigated brain regions in comparison to the control rats (Table 4). Interestingly, similar decrement of the brain AC was found following the combined TG+STZ-icv treatment, i.e. the values of ORAC- OH were also significantly decreased in all three investigated brain regions in comparison to the control ones while those of ORAC- ROO remained unchanged (Table 4). Table 4. Antioxidant capacity against hydroxyl- (ORAC -OH ) and peroxyl- radical (ORAC - ROO ) in different regions of the rat brain three months following the intracerebroventricular treatment of streptozotocin, glucose transport inhibitor 5-thio-D-glucose and their combination, respectively.
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  • Summer '07
  • HARRIS-WARRICK,R.M.
  • Diabetes, Blood sugar, oxidative stress, Diabetic neuropathy

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