|
NISCAIR ONLINE PERIODICALS REPOSITORY (NOPR) >
NISCAIR PUBLICATIONS >
Research Journals >
Indian Journal of Biochemistry and Biophysics (IJBB) >
IJBB Vol.49 [2012] >
IJBB Vol.49(5) [October 2012] >
| Title: | Effect of aluminum exposure on superoxide and peroxide handling capacities by liver, kidney, testis and temporal cortex in rat |
| Authors: | Chaitanya, T V Balasai
Mallipeddi, Kalyani
Bondili, J S
Nayak, Prasunpriya |
| Keywords: | Aluminum
Catalase
GPx
GR
GSH
Kidney
Liver
SOD
Superoxide peroxide handling capacity
Temporal cortex
Testis |
| Issue Date: | Oct-2012 |
| Publisher: | NISCAIR-CSIR, India |
| Abstract: | Oxidant imbalance is one of the causative
mechanisms of aluminum-induced neurotoxicity. In this study, we investigated
aluminum-induced oxidant imbalance in non-neuronal tissues (liver, kidney and
testis) and temporal cortex in rats. The differences in adaptations to
superoxide and peroxide handling capacities (SPHC) of studied organs due to
aluminum insult were also evaluated. Male Wistar rats were exposed to aluminum
(10 mg/Kg body wt/day) for 4 weeks through orogastric intubation. Liver showed
significant decrease in reduced glutathione level, while significant alteration
in lipid peroxidation was observed in temporal cortex in aluminium-exposed
animals. Superoxide dismutase activity was significantly altered in liver and
temporal cortex and catalase activity significantly reduced in the liver due to
aluminum exposure, while glutathione reductase and glutathione peroxidase
activities were altered in all the tested organs. Among the organs,
glutathione-independent SPHC was relatively higher in liver and kidney, while
glutathione-dependent SPHC was relatively higher in testis and temporal cortex.
As compared to control, aluminum-exposed rats demonstrated reduction in
glutathione-dependent SPHC in temporal cortex and increment of the same in
testis, while increment in glutathione-independent SPHC was observed in liver.
In conclusion, aluminum-induced alteration in oxidant handling capacity could
be the cause of oxidative stress both in the neuronal and
non-neuronal tissues. |
| Page(s): | 395-398 |
| CC License: |  CC Attribution-Noncommercial-No Derivative Works 2.5 India |
| ISSN: | 0975-0959 (Online); 0301-1208 (Print) |
| Source: | IJBB Vol.49(5) [October 2012]
|
|
