This 2013 review by Michael J. Kosnett evaluates the efficacy of chelation therapy for metal poisonings beyond the commonly treated lead, arsenic, and mercury. The paper highlights that while chelation is established for acute exposures to certain metals, its utility in chronic toxicity is often unsupported due to limited evidence.
This longitudinal study by Gulson et al., published in Archives of Toxicology (2016), investigates the dynamics of lead mobilization from maternal bone stores during pregnancy and its subsequent transfer to the fetus. Utilizing monthly blood sampling and isotopic analysis, the researchers tracked lead levels in 15 pregnant women from early
This 2013 commentary by Mary Jean Brown, published in the Journal of Medical Toxicology, addresses the complexities of administering chelation therapy to pregnant women with lead poisoning. The article emphasizes that while chelation can effectively reduce maternal blood lead levels, it may inadvertently increase fetal exposure by mobilizing lead from
This 1986 study by Brownie et al., published in Toxicology and Applied Pharmacology, investigated the teratogenic potential of calcium edetate (CaEDTA), a chelating agent used in lead poisoning treatment, when administered to pregnant rats during organogenesis. The researchers administered varying doses of CaEDTA (2, 4, 6, and 8 mmol/m²/day) and
This 2001 review by Vinceti et al., published in Reviews on Environmental Health, synthesizes epidemiological studies and case reports to elucidate the toxicological profile of selenium in humans. The authors highlight that chronic exposure to selenium compounds, particularly at dietary intakes around 300 µg/day, can disrupt endocrine functions, notably impairing
This 1994 study by Yang and Zhou, published in the Journal of Trace Elements and Electrolytes in Health and Disease, investigates the maximum safe dietary selenium intake among residents in a selenium-rich region of China. The researchers re-examined five individuals previously diagnosed with selenosis, characterized by symptoms like nail and
This 2013 review by Sikiric et al. explores the protective effects of the stable gastric pentadecapeptide BPC 157 against nonsteroidal anti-inflammatory drug (NSAID)-induced toxicity. NSAIDs, while effective for pain and inflammation, are associated with gastrointestinal (GI) and systemic adverse effects, including ulcers, bleeding, and organ damage. The authors present evidence
This 2006 study by Boban-Blagaic et al. investigated the effects of BPC 157, a stable gastric pentadecapeptide, on acute and chronic ethanol-induced toxicity in mice, and its interaction with the nitric oxide (NO) system. In the acute model, mice received 4 g/kg of ethanol intraperitoneally, leading to anesthesia, hypothermia, elevated
This 2010 preclinical study by Ilic et al., published in the Journal of Physiology and Pharmacology, investigated the protective effects of the stable gastric pentadecapeptide BPC 157 against severe paracetamol-induced toxicity in rats. Administering a high hepatotoxic dose of paracetamol (5 g/kg intraperitoneally) led to rapid onset of generalized convulsions,
This 2009 preclinical study, published in Regulatory Peptides, investigated the cardioprotective effects of the pentadecapeptide BPC 157 on methyldigoxin-induced arrhythmias in rats, focusing on the involvement of the nitric oxide (NO) system. Methyldigoxin, a cardiac glycoside, is known to cause arrhythmias at toxic doses. The study found that BPC 157
