Therapeutic potential of monoisoamyl and monomethyl esters of meso 2,3-dimercaptosuccinic acid in gallium arsenide intoxicated rats

Flora, Swaran J.S.; Mehta, Ashish; Rao, P. Venkata; Kannan, G. M.; Bhaskar, A.S.B.; Dube, S. N.; Pant, B. P.

doi:10.1016/j.tox.2003.09.010

Cited by 50 publications

(37 citation statements)

References 67 publications

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“…MiADMSA completely prevented testicular damage after intraperitoneal administration of cadmium chloride at a dose of 0.03 mmol/kg 67) . Recently, Flora et al reported the effect of MiADMSA on the reversal of gallium arsenide (GaAs) induced changes in hepatic tissue 79,80) Rats were exposed for 24 wk to 10 mg/kg GaAs, orally, once daily and treated with 0.3 mmol/kg of MiADMSA or DMSA for two courses. They observed that MiADMSA was better than DMSA in mobilizing arsenic and in the turnover of the GaAs sensitive biochemical variables.…”

Section: Monoisoamyl Dmsa (Miadmsa)mentioning

confidence: 99%

Strategies for Safe and Effective Therapeutic Measures for Chronic Arsenic and Lead Poisoning

Kalia¹,

Flora²

2005

Journal of Occupational Health

269

161

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Strategies for Safe and Effective Therapeutic Measures for Arsenic and LeadPoisoning: Kiran Kalia, et al. Department of Biosciences, Sardar Patel University, IndiaExposure to toxic metals remains a widespread occupational and environmental problem in world. There have been a number of reports in the recent past suggesting an incidence of childhood lead poisoning and chronic arsenic poisoning due to contaminated drinking water in many areas of West Bengal in India and Bangladesh has become a national calamity. Low level metal exposure in humans is caused by air, food and water intake. Lead and arsenic generally interferes with a number of body functions such as the central nervous system (CNS), the haematopoietic system, liver and kidneys. Over the past few decades there has been growing awareness and concern that the toxic biochemical and functional effects are occurring at a lower level of metal exposure than those that produce overt clinical and pathological signs and symptoms. Despite many years of research, we are still far from an effective treatment of chronic plumbism and arsenicosis. Medical treatment of acute and chronic lead and arsenic toxicity is furnished by chelating agents. Chelating agents are organic compounds capable of linking together metal ions to form complex ring-like structures called chelates. They have been used clinically as antidotes for acute and chronic poisoning. 2, 3-dimercaprol (BAL) has long been the mainstay of chelation therapy for lead or arsenic poisoning. Meso 2, 3, -dimercaptosuccinic acid (DMSA) has been tried successfully in animals as well as in a few cases of human lead and arsenic poisoning. DMSA could be a safe and effective method for treating lead or arsenic poisoning, but one of the major disadvantages of chelation with DMSA has been its Review inability to remove lead from the intracellular sites because of its lipophobic nature. Further, it does not provide protection in terms of clinical/ biochemical recovery. A new trend in chelation therapy is to use combined treatment. This includes the use of structurally different chelators or a combination of an adjuvant and a chelator to provide better clinical/ biochemical recovery in addition to lead mobilization. The present review article attempts to provide update information about the current strategies being adopted for a safe, effective and specific treatment for two major toxic metals or metalloid.

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Section: Monoisoamyl Dmsa (Miadmsa)mentioning

confidence: 99%

Strategies for Safe and Effective Therapeutic Measures for Chronic Arsenic and Lead Poisoning

Kalia¹,

Flora²

2005

Journal of Occupational Health

269

161

View full text Add to dashboard Cite

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“…Recently, a number of mono and diesters of DMSA were synthesized and tested for metal intoxication, especially against lead (Pande and Flora, 2002;Saxena et al, 2005;Saxena and Flora, 2006), cadmium (Xu et al, 1995), mercury (Blanusa et al, 1997), and gallium arsenide (Flora, 1999;Flora et al, 2004). Among these monoesters, MiADMSA ( Fig.…”

mentioning

confidence: 99%

Reversal of Lead-Induced Neuronal Apoptosis by Chelation Treatment in Rats: Role of Reactive Oxygen Species and Intracellular Ca²⁺

Flora¹,

Saxena²,

Mehta³

2007

J Pharmacol Exp Ther

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154

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Lead, a ubiquitous and potent neurotoxicant causes several neurophysiological and behavioral alterations. Toxic properties of lead have been attributed to its capability to mimic calcium and alter calcium homeostasis. In this study, we have addressed the following issues: 1) whether chelation therapy could circumvent the altered Ca 2ϩ homeostasis and prevent neuronal death in chronic lead-intoxicated rats, 2) whether chelation therapy could revert altered biochemical and behavioral changes, 3) whether combinational therapy using two different chelating agents was more advantageous over monotherapy in lead-treated rats, and 4) what could be the mechanism of neuronal apoptosis. Results indicated that lead caused a significant increase in reactive oxygen species, neuronal nitric-oxide synthetase, and intracellular free calcium levels along with altered behavioral abnormalities in locomotor activity, exploratory behavior, learning, and memory that were supported by changes in neurotransmitter levels. A fall in membrane potential, release of cytochrome c, and altered bcl 2 /bax ratio indicated mitochondrial-dependent apoptosis. Most of these alterations reverted toward normal level following combination therapy over monotherapy with calcium disodium EDTA (CaNa 2 EDTA) or monoisoamyl meso-2,3-dimercaptosuccinic acid (MiADMSA). It could be concluded from our present results that combined therapy with CaNa 2 EDTA and MiADMSA might be a better treatment protocol than monotherapy with these chelators in lead-induced neurological disorders. We for the first time report the role of Ca 2ϩ in regulating neurological dystrophy caused by chronic lead exposure in rats and its recovery with a two-course treatment regime of mono or combination therapy.

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“…Two studies of Flora et al [31,32] are included in this study. Significant DNA damage was assessed in mice [32], while in rats no data was reported [31].…”

Section: Detail Description Of Findingsmentioning

confidence: 99%

“…Two studies of Flora et al [31,32] are included in this study. Significant DNA damage was assessed in mice [32], while in rats no data was reported [31]. Similar extent of DNA damage was observed in children living in mining site of Villa de Paz with high arsenic contamination compared with children living in Matechuala with low arsenic contamination [33].…”

Section: Detail Description Of Findingsmentioning

confidence: 99%

Assessment of Arsenic Induced DNA Fragmentation by using Comet Assay

Mahjabeen¹

2016

J Carcinog Mutagen

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Arsenic is metalloid present in measureable quantity in air, water, and soil through natural and anthropogenic sources. It is neurotoxic, hepatotoxic and genotoxic effects, variety of health problems have been associated to arsenic exposure. This review was designed to investigate the possible association between arsenic exposure and DNA damage in animals and humans using comet assay. Total 28 studies were selected for measuring DNA damage by comet assay. Trend of significance in tail length and tail moment was observed using regression analysis. Due to limited number of studies available the regression analysis was non-significant. Individually each study suggested a significant increase in tail moment and tail length in a dose and time-dependent manner. Overall trend observed in this review is the positive association between arsenic exposure either experimentally or occupationally and DNA damage. This initial effort may provide future guideline for the assessment of DNA fragmentation using comet assay.

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Therapeutic potential of monoisoamyl and monomethyl esters of meso 2,3-dimercaptosuccinic acid in gallium arsenide intoxicated rats

Cited by 50 publications

References 67 publications

Strategies for Safe and Effective Therapeutic Measures for Chronic Arsenic and Lead Poisoning

Strategies for Safe and Effective Therapeutic Measures for Chronic Arsenic and Lead Poisoning

Reversal of Lead-Induced Neuronal Apoptosis by Chelation Treatment in Rats: Role of Reactive Oxygen Species and Intracellular Ca²⁺

Assessment of Arsenic Induced DNA Fragmentation by using Comet Assay

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Therapeutic potential of monoisoamyl and monomethyl esters of meso 2,3-dimercaptosuccinic acid in gallium arsenide intoxicated rats

Cited by 50 publications

References 67 publications

Strategies for Safe and Effective Therapeutic Measures for Chronic Arsenic and Lead Poisoning

Strategies for Safe and Effective Therapeutic Measures for Chronic Arsenic and Lead Poisoning

Reversal of Lead-Induced Neuronal Apoptosis by Chelation Treatment in Rats: Role of Reactive Oxygen Species and Intracellular Ca2+

Assessment of Arsenic Induced DNA Fragmentation by using Comet Assay

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Reversal of Lead-Induced Neuronal Apoptosis by Chelation Treatment in Rats: Role of Reactive Oxygen Species and Intracellular Ca²⁺