Issue 43, 2013

Aluminium induced metabolic changes in kidney and heart tissue of mice: a Fourier transform infrared spectroscopy study

Abstract

In this study, we aimed to evaluate aluminium induced metabolic changes in kidney and heart tissues of mice using Fourier transform infrared spectroscopy analysis. This result revealed the alterations on the major biochemical constituents, such as lipids, proteins and nucleic acids of the kidney tissues of mice. In aluminium intoxicated kidney tissue significant shift and decrease in the area value of the amide A band and decrease in protein-to-lipid ratio indicated quantitative and qualitative alterations in the protein profile due to iron-initiated free radical formation. Shift in the peak position of the PO2 asymmetric stretching band for aluminium intoxicated kidney tissue indicated the dehydrated phosphate group. This might be due to the binding of aluminium with phosphate or interruption of aluminium in calcium metabolism. The increased level of serum uric acid might have resulted from the essential hypertension, which might be due to marked accumulation of O2˙ in the kidney. All of the above mentioned modifications were protected in Desferrioxamine treated mice. The overall findings exhibited that aluminium toxicity might induce essential hypertension through the dysfunction of kidneys. The results of the FTIR study were found to be in agreement with biochemical studies which demonstrated that FTIR could be used successfully to indicate the molecular level changes.

Graphical abstract: Aluminium induced metabolic changes in kidney and heart tissue of mice: a Fourier transform infrared spectroscopy study

Article information

Article type
Paper
Submitted
02 Jun 2013
Accepted
04 Sep 2013
First published
04 Sep 2013

RSC Adv., 2013,3, 20896-20904

Aluminium induced metabolic changes in kidney and heart tissue of mice: a Fourier transform infrared spectroscopy study

S. Sivakumar, J. Sivasubramanian, C. Prasad khatiwada, J. Manivannan and B. Raja, RSC Adv., 2013, 3, 20896 DOI: 10.1039/C3RA42714E

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