Arsenic (As) Contamination in Different Food and Dietary Samples from Several Districts of Bangladesh and Arsenic (As) Detection, Mitigation and Toxicity Measurement and impact of Dietary Arsenic Exposure on Human Health

Objective: To determine the level of arsenic concentration in vegetables and other food categories in three selected areas of Pabna district and to estimate quantitatively the dietary arsenic exposure in one of the arsenic contaminated areas of Bangladesh.Materials and Methods: The study was conducted in CharRuppur, Char mirkamari and Lakshmikunda village of IshwardiUpzila in Pabna district. Ishwardi (Town) consists of 12 wardsand 37 mahallas. Arsenic was detected in the ADM Lab,Department of Pharmacology, Bangladesh Agricultural University, Mymensingh with Hydride Generation Atomic Absorption Spectrophotometer (HG-AAS; PG-990, PG Instruments Ltd. UK). Arsenic was detected by forming AsH3 at below pH 1.0 after the reaction of As with a solution of sodiumborohydride (NaBH4), sodium hydroxide (NaOH, M=40,000g/mol,) and 10% HCl. In this test, standard was maintained asAsV ranging from 0 to 12.5 μg/L.Results: A total of 120 vegetable samples, 15 rice samples and15 fish samples were collected from five different markets ofthree different villages of Pabna district and were tested forarsenic concentration. Findings demonstrated that the mean concentration of As in leafy vegetables (0.52 μg g-1) was significantly higher compared to those found in fruity (0.422μg g-1) and root & tuber vegetables (0.486 μg g-1).Conclusion: Underground Contaminated water was the major source for the As contamination of various products in Pabna.The arsenic levels were found higher among the leafy vegetables samples in comparison to fruit and root & tuber vegetables. Further studies will be conducted to search the genetic risk factors of arsenic toxicity in the population of the mostly affected people

Hyper-inflammation and skin destruction mediated by rosiglitazone activation of macrophages in IL-6 deficiency

Injury initiates recruitment of macrophages to support tissue repair; however, excessive macrophage activity may exacerbate tissue damage causing further destruction and subsequent delay in wound repair. Here we show that the peroxisome proliferation–activated receptor-γ agonist, rosiglitazone (Rosi), a medication recently reintroduced as a drug to treat diabetes and with known anti-inflammatory properties, paradoxically generates pro-inflammatory macrophages. This is observed in both IL-6-deficient mice and control wild-type mice experimentally induced to produce high titers of auto-antibodies against IL-6, mimicking IL-6 deficiency in human diseases. IL-6 deficiency when combined with Rosi-mediated upregulation of suppressor of cytokine signaling 3 leads to an altered ratio of nuclear signal transducer and activator of transcription 3/NF-κB that allows hyper-induction of inducible nitric oxide synthase (iNOS). Macrophages activated in this manner cause de novo tissue destruction, recapitulating human chronic wounds, and can be reversed in vivo by recombinant IL-6, blocking macrophage infiltration, or neutralizing iNOS. This study provides insight into an unanticipated paradoxical role of Rosi in mediating hyper-inflammatory macrophage activation significant for diseases associated with IL-6 deficiency