PMID- 23420078
OWN - NLM
STAT- MEDLINE
DCOM- 20140212
LR  - 20211021
IS  - 1559-1182 (Electronic)
IS  - 0893-7648 (Linking)
VI  - 48
IP  - 1
DP  - 2013 Aug
TI  - Zinc, a neuroprotective agent against aluminum-induced oxidative DNA injury.
PG  - 1-12
LID - 10.1007/s12035-013-8417-7 [doi]
AB  - Aluminum (Al) has been considered as one of the most abundant elements and 
      comprises nearly 8 % of the Earth's crust. Despite of its immense presence, 
      studies regarding the molecular basis of its interaction with the physiological 
      system are rather sparse. On the other hand, zinc (Zn), an essential 
      micronutrient, has been regarded as the second most important metal for brain 
      functioning. The objective of the present study was to investigate the protective 
      potential of Zn, if any, during Al-induced detrimental effects on DNA, tritiated 
      thymidine uptake as well as expression of stress marker genes and proteins in rat 
      brain. Male Sprague-Dawley rats weighing 140-160 g were divided into four 
      different groups viz.: normal control, Al treated (100 mg/kg b wt/day via oral 
      gavage), Zn treated (227 mg/l in drinking water), and combined Al and Zn treated. 
      All the treatments were carried out for a total duration of 8 weeks. Agarose gel 
      electrophoresis revealed DNA laddering pattern and comets in the rat brain 
      following Al treatment, which however, were attenuated upon Zn treatment. 
      Further, terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling 
      (TUNEL)-positive cells, number of apoptotic brain cells, and uptake of tritiated 
      thymidine were increased after Al treatment but were decreased upon Zn 
      supplementation. Western blot and mRNA expressions of p53 and nuclear factor kappaB 
      (NF-kappaB) were also found to be significantly elevated after Al treatment, which 
      however, were reversed following Zn treatment. Hence, Zn shall prove to be an 
      effective agent in mitigating the detrimental effects caused by Al in the rat 
      brain.
FAU - Singla, Neha
AU  - Singla N
AD  - Department of Biophysics, Panjab University, Chandigarh, 160014, India.
FAU - Dhawan, D K
AU  - Dhawan DK
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20130219
PL  - United States
TA  - Mol Neurobiol
JT  - Molecular neurobiology
JID - 8900963
RN  - 0 (NF-kappa B)
RN  - 0 (Neuroprotective Agents)
RN  - 0 (Tumor Suppressor Protein p53)
RN  - 10028-17-8 (Tritium)
RN  - 9007-49-2 (DNA)
RN  - CPD4NFA903 (Aluminum)
RN  - J41CSQ7QDS (Zinc)
RN  - VC2W18DGKR (Thymidine)
SB  - IM
MH  - Aluminum/*toxicity
MH  - Animals
MH  - Apoptosis/drug effects
MH  - Cerebellum/drug effects/metabolism
MH  - Cerebrum/drug effects/metabolism
MH  - Comet Assay
MH  - DNA/isolation & purification
MH  - *DNA Damage
MH  - DNA Fragmentation/drug effects
MH  - Densitometry
MH  - Electrophoresis, Agar Gel
MH  - In Situ Nick-End Labeling
MH  - Male
MH  - Microscopy, Fluorescence
MH  - NF-kappa B/metabolism
MH  - Neuroprotective Agents/*pharmacology
MH  - Oxidative Stress/*drug effects
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - Thymidine/metabolism
MH  - Tritium/metabolism
MH  - Tumor Suppressor Protein p53/metabolism
MH  - Zinc/*pharmacology
EDAT- 2013/02/20 06:00
MHDA- 2014/02/13 06:00
CRDT- 2013/02/20 06:00
PHST- 2012/10/02 00:00 [received]
PHST- 2013/01/29 00:00 [accepted]
PHST- 2013/02/20 06:00 [entrez]
PHST- 2013/02/20 06:00 [pubmed]
PHST- 2014/02/13 06:00 [medline]
AID - 10.1007/s12035-013-8417-7 [doi]
PST - ppublish
SO  - Mol Neurobiol. 2013 Aug;48(1):1-12. doi: 10.1007/s12035-013-8417-7. Epub 2013 Feb 
      19.