Stojanovic, Srdan D.

Link to this page

Authority KeyName Variants
orcid::0000-0002-1847-9318
  • Stojanovic, Srdan D. (1)
Projects

Author's Bibliography

CaNa(2)EDTA chelation attenuates cell damage in workers exposed to lead-a pilot study

Čabarkapa-Pirković, Andrea ; Borozan, Sunčica Z.; Živković, Lada; Stojanovic, Srdan D.; Milanović-Čabarkapa, Mirjana; Bajić, Vladan P.; Spremo-Potparević, Biljana

(Elsevier, 2015)

TY  - JOUR
AU  - Čabarkapa-Pirković, Andrea 
AU  - Borozan, Sunčica Z.
AU  - Živković, Lada
AU  - Stojanovic, Srdan D.
AU  - Milanović-Čabarkapa, Mirjana
AU  - Bajić, Vladan P.
AU  - Spremo-Potparević, Biljana
PY  - 2015
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/873
AB  - Lead induced oxidative cellular damage and long-term persistence of associated adverse effects increases risk of late-onset diseases. CaNa(2)EDTA chelation is known to remove contaminating metals and to reduce free radical production. The objective was to investigate the impact of chelation therapy on modulation of lead induced cellular damage, restoration of altered enzyme activities and lipid homeostasis in peripheral blood of workers exposed to lead, by comparing the selected biomarkers obtained prior and after five-day CaNa(2)EDTA chelation intervention. The group of smelting factory workers diagnosed with lead intoxication and current lead exposure 5.8 +/- 1.2 years were administered five-day CaNa(2)EDTA chelation. Elevated baseline activity of antioxidant enzymes Cu, Zn-SOD and CAT as well as depleted thiols and increased protein degradation products-carbonyl groups and nitrites, pointing to Pb induced oxidative damage, were restored toward normal values following the treatment. Lead showed inhibitor potency on both RBC AChE and BChE in exposed workers, and chelation re-established the activity of BChE, while RBC AChE remained unaffected. Also, genotoxic effect of lead detected in peripheral blood lymphocytes was significantly decreased after therapy, exhibiting 18.9% DNA damage reduction. Administration of chelation reversed the depressed activity of serum PON 1 and significantly decreased lipid peroxidation detected by the post-chelation reduction of MDA levels. Lactate dehydrogenase LDF1-5 isoenzymes levels showed evident but no significant trend of restoring toward normal control values following chelation. CaNa(2)EDTA chelation ameliorates the alterations linked with Pb mediated oxidative stress, indicating possible benefits in reducing health risks associated with increased oxidative damage in lead exposed populations. (C) 2015 Elsevier Ireland Ltd. All rights reserved.
PB  - Elsevier
T2  - Chemico-Biological Interactions
T1  - CaNa(2)EDTA chelation attenuates cell damage in workers exposed to lead-a pilot study
VL  - 242
SP  - 171
EP  - 178
DO  - 10.1016/j.cbi.2015.10.002
ER  - 
@article{
author = "Čabarkapa-Pirković, Andrea  and Borozan, Sunčica Z. and Živković, Lada and Stojanovic, Srdan D. and Milanović-Čabarkapa, Mirjana and Bajić, Vladan P. and Spremo-Potparević, Biljana",
year = "2015",
abstract = "Lead induced oxidative cellular damage and long-term persistence of associated adverse effects increases risk of late-onset diseases. CaNa(2)EDTA chelation is known to remove contaminating metals and to reduce free radical production. The objective was to investigate the impact of chelation therapy on modulation of lead induced cellular damage, restoration of altered enzyme activities and lipid homeostasis in peripheral blood of workers exposed to lead, by comparing the selected biomarkers obtained prior and after five-day CaNa(2)EDTA chelation intervention. The group of smelting factory workers diagnosed with lead intoxication and current lead exposure 5.8 +/- 1.2 years were administered five-day CaNa(2)EDTA chelation. Elevated baseline activity of antioxidant enzymes Cu, Zn-SOD and CAT as well as depleted thiols and increased protein degradation products-carbonyl groups and nitrites, pointing to Pb induced oxidative damage, were restored toward normal values following the treatment. Lead showed inhibitor potency on both RBC AChE and BChE in exposed workers, and chelation re-established the activity of BChE, while RBC AChE remained unaffected. Also, genotoxic effect of lead detected in peripheral blood lymphocytes was significantly decreased after therapy, exhibiting 18.9% DNA damage reduction. Administration of chelation reversed the depressed activity of serum PON 1 and significantly decreased lipid peroxidation detected by the post-chelation reduction of MDA levels. Lactate dehydrogenase LDF1-5 isoenzymes levels showed evident but no significant trend of restoring toward normal control values following chelation. CaNa(2)EDTA chelation ameliorates the alterations linked with Pb mediated oxidative stress, indicating possible benefits in reducing health risks associated with increased oxidative damage in lead exposed populations. (C) 2015 Elsevier Ireland Ltd. All rights reserved.",
publisher = "Elsevier",
journal = "Chemico-Biological Interactions",
title = "CaNa(2)EDTA chelation attenuates cell damage in workers exposed to lead-a pilot study",
volume = "242",
pages = "171-178",
doi = "10.1016/j.cbi.2015.10.002"
}
Čabarkapa-Pirković, A., Borozan, S. Z., Živković, L., Stojanovic, S. D., Milanović-Čabarkapa, M., Bajić, V. P.,& Spremo-Potparević, B.. (2015). CaNa(2)EDTA chelation attenuates cell damage in workers exposed to lead-a pilot study. in Chemico-Biological Interactions
Elsevier., 242, 171-178.
https://doi.org/10.1016/j.cbi.2015.10.002
Čabarkapa-Pirković A, Borozan SZ, Živković L, Stojanovic SD, Milanović-Čabarkapa M, Bajić VP, Spremo-Potparević B. CaNa(2)EDTA chelation attenuates cell damage in workers exposed to lead-a pilot study. in Chemico-Biological Interactions. 2015;242:171-178.
doi:10.1016/j.cbi.2015.10.002 .
Čabarkapa-Pirković, Andrea , Borozan, Sunčica Z., Živković, Lada, Stojanovic, Srdan D., Milanović-Čabarkapa, Mirjana, Bajić, Vladan P., Spremo-Potparević, Biljana, "CaNa(2)EDTA chelation attenuates cell damage in workers exposed to lead-a pilot study" in Chemico-Biological Interactions, 242 (2015):171-178,
https://doi.org/10.1016/j.cbi.2015.10.002 . .
10
7
9