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Management of Trace Elements in Short Bowel Syndrome
Published in John K. DiBaise, Carol Rees Parrish, Jon S. Thompson, Short Bowel Syndrome Practical Approach to Management, 2017
Chromium toxicity is a greater concern than deficiency in patients who receive long-term PN, especially in pediatric patients [4,49]. The chromium provided in multiple trace element formulations, combined with contamination of PN components during their manufacture, provides excessive chromium [4,49]. Patients receiving long-term PN may have elevated serum chromium, and increased tissue deposition of chromium has been reported [4,49]. Excessive serum chromium has been associated with compromised renal function in PN-dependent pediatric patients, and although no cases of overt chromium toxicity have been reported, tissue levels of chromium are elevated after extended PN use [49,50]. Routine monitoring of blood chromium is generally not recommended because the concentration of chromium in the serum is so minimal that an accurate measurement with the possibility of contamination in normal clinical settings makes the results unreliable [4].
The possible protective role of vitamin C versus melatonin on potassium dichromate induced changes in rat thyroid gland: light and electron microscopic study
Published in Ultrastructural Pathology, 2023
Eman Saeed, Ahmed A. El-Mansy, Shireen A Mazroa, Amal M. Moustafa
Many studies revealed a significant reduction of glutathione (GSH) concentration in the cells of hexavalent chromium-treated rats, with an increase in the contents of catalase within the cells.33,44,45 Furthermore, potassium dichromate was found to increase serum TNF- and interleukin-6 (IL-6) concentrations, which are inflammatory cytokines produced in response to chromium-induced ROS species formation. Those inflammatory mediators cause destruction of the thyroid gland with decreased serum levels of free T3 and T4.38,46 Chromium toxicity may result in hypothyroidism, as evidenced by an increase in serum TSH and a decrease in serum T3 and T4 concentrations (Table 2). Circulating T4 and T3 levels act as useful biomarkers of potential effects on the thyroid gland. Serum levels of T4 and T3 could be used as a good reflection of the functional state of the thyroid gland in both humans and experimental animals. Although chromium was shown to increase the production of thyroglobulin, it decreased the release of thyroid hormones from the thyroglobulin by hindering the process of proteolysis of thyroglobulin, with the reduction in their free serum concentrations.47
An adverse outcome pathway for small intestinal tumors in mice involving chronic cytotoxicity and regenerative hyperplasia: a case study with hexavalent chromium, captan, and folpet
Published in Critical Reviews in Toxicology, 2020
Virunya S. Bhat, Samuel M. Cohen, Elliot B. Gordon, Charles E. Wood, John M. Cullen, Mark A. Harris, Deborah M. Proctor, Chad M. Thompson
Various regulatory authorities have accepted a cytotoxicity-mediated regenerative hyperplasia-based MOA for Cr(VI), captan, and folpet (U.S. EPA 2004, 2012; Health Canada 2016; FSCJ 2017, 2019). For Cr(VI), Health Canada (2016) noted that no studies have identified the essentiality of early KEs (i.e. studies measuring the presence or absence of tumors after one of the early KEs, such as cytotoxicity, is prevented). However, there is evidence of reversibility in shorter-term bioassays, an absence of genotoxicity in the target tissue, and consistent and reproducible non-neoplastic lesions in the duodenum. While no major gaps in the MOA were identified, Health Canada (2016) noted that additional measures might provide more detailed mechanistic understanding of (1) Cr(III) and Cr(VI) speciation in biological samples, (2) oxidative status (in addition to GSH/GSSG) in SI epithelial tissues, (3) differentiation of chromium–DNA adducts between crypt and villi enterocytes in vivo, and (4) DNA methylation. Health Canada (2016) noted that although this type of information might provide useful context for chromium toxicity, it would not change the non-mutagenic MOA. Health Canada (2016) considered the lack of mutagenicity in target tissues to be a major weakness in the WOE supporting a mutagenic MOA. No significant gaps of weaknesses in the MOA were noted by regulators for captan or folpet. Overall, while there are no perceived significant gaps or weaknesses in the KEs or KERs supporting this AOP, identification of the exact molecular mechanisms underlying cytotoxicity as the (M)IE would better conform to the AOP framework; however, it is not clear to these authors that cytotoxic MOAs/AOPs necessarily have a single MIE.