Therapeutic Profile of T11TS vs. T11TS+MiADMSA: A Hunt for a More Effective Therapeutic Regimen for Arsenic Exposure

  • Chaudhuri, Suhnrita (Department of Laboratory Medicine, School of Tropical Medicine) ;
  • Acharya, Sagar (Department of Laboratory Medicine, School of Tropical Medicine) ;
  • Chatterjee, Sirshendu (Department of Laboratory Medicine, School of Tropical Medicine) ;
  • Kumar, Pankaj (Department of Laboratory Medicine, School of Tropical Medicine) ;
  • Singh, Manoj Kumar (Department of Laboratory Medicine, School of Tropical Medicine) ;
  • Bhattacharya, Debanjan (Department of Biochemistry and Medical Biotechnology, School of Tropical Medicine) ;
  • Basu, Anjan Kumar (Division of Pharmacology & Toxicology, Defence Research & Development Establishment) ;
  • Dasgupta, Shyamal (Department of Laboratory Medicine, School of Tropical Medicine) ;
  • Flora, S.J.S. (Division of Pharmacology & Toxicology, Defence Research & Development Establishment) ;
  • Chaudhuri, Swapna (Department of Laboratory Medicine, School of Tropical Medicine)
  • Published : 2012.06.30


Arsenic exposure is a serious health hazard worldwide. We have previously established that it may result in immune suppression by upregulating Th2 cytokines while downregulating Th1 cytokines and causing lymphocytic death. Treatment modalities for arsenic poisoning have mainly been restricted to the use of chelating agents in the past. Only recently have combination therapies using a chelating agent in conjunction with other compounds such as anti-oxidants, micronutrients and various plant products, been introduced. In the present study, we used T11TS, a novel immune potentiating glycopeptide alone and in combination with the sulfhydryl-containing chelator, mono-iso-amyl-dimarcaptosuccinic acid (MiADMSA) as a therapeutic regimen to combat arsenic toxicity in a mouse model. Results indicated that Th1 cytokines such as TNF-${\alpha}$, $IFN{\gamma}$, IL12 and the Th2 cytokines such as IL4, IL6, IL10 which were respectively downregulated and upregulated following arsenic induction were more efficiently restored to their near normal levels by T11TS alone in comparison with the combined regimen. Similar results were obtained with the apoptotic proteins studied, FasL, BAX, BCL2 and the caspases 3, 8 and 9, where again T11TS proved more potent than in combination with MiADMSA in preventing lymphocyte death. The results thus indicate that T11TS alone is more efficient in immune re-establishment after arsenic exposureas compared to combination therapy with T11TS+MiADMSA.


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