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Inhalation Toxicity of Metal Particles and Vapors
Published in Jacob Loke, Pathophysiology and Treatment of Inhalation Injuries, 2020
Although absorption is highly dependent on the chemical and physical form of the inhaled arsenic compounds, the common forms (particularly arsenic trioxide, the most prevalent) are fully absorbed from the lungs and mucous surfaces of the respiratory tract. It is generally true that trivalent arsenic compounds (arsenites) are more toxic than pentavalent compounds and that natural oxidation factors the conversion of trivalent arsenic to the pentavalent form.
Biochemical Aspects of Fatty Liver
Published in Robert G. Meeks, Steadman D. Harrison, Richard J. Bull, Hepatotoxicology, 2020
The hypothesis has also been advanced that fatty liver following arsenite poisoning is related to a block in fatty acid oxidation. Intraperitoneal injection of 25 mg/kg b.w. As2O3 provokes within half an hour a strong decrease in oxidations in the liver (Webb, 1966). According to this author, the damage would follow the interaction of As3+ with the -SH groups of lipoic acid, which is involved in fatty acid oxidation. Dihydrolipoate dehydrogenase has been found to be inhibited. In principle, As3+ might even act on other -SH groups, as those required for protein synthesis. Thus, fat accumulation might be dependent on a block in lipoprotein synthesis, at least in the late stages of poisoning.
Reactivities of Amino Acids and Proteins with Iodine
Published in Erwin Regoeczi, Iodine-Labeled Plasma Proteins, 2019
The reagent is composed of two solutions which are mixed at equal proportion immediately before use. Solution A is ceric sulfate (10% w/v), obtained by dissolving 10 g Ce(SO4)2 ·4H20 in 100 m𝓁 of cold (0 to 5°C), 1M H2SO4; after 1 hr of refrigeration, the solution is clarified by centrifugation. Solution B is prepared by dissolving 5 g NaAsO2 in 100 m𝓁 of cold, 1 M H2SO4. The arsenite is added in small portions under vigorous stirring to avoid precipitation of arsenious oxide.
Profiles and potential health risks of heavy metals in polluted soils in NE-Iran
Published in Toxin Reviews, 2022
Masumeh Taheri, Mohamad Hosein Mahmudy Gharaie, Jalil Mehrzad, Michael Stone, Reza Afshari
Sediment-associated metals in many regions of the world represent a significant health concern for humans as well as terrestrial and aquatic biota (Tyler et al. 1989, Rotkin et al. 2010, Kahlon et al. 2018, He et al. 2019). The bioavailability and toxicity of metals depends on several environmental factors as well as the physicochemical characteristics of soils and the specific metal (Violante et al. 2010). For example, inorganic forms of As such as arsenate and arsenite are more toxic than methylated As (Huang and Matzner 2007). The toxicity of arsenite is 25–60 times greater than arsenate and it has been shown to be highly mobile in the environment (Corwin et al. 1999, Wang and Mulligan 2006). Metal contamination in soil (surface and subsurface) can represent a significant source and pathway affecting both ecosystem and human health (Roychowdhury et al. 2002, Li and Ji 2017). The most common pathway of metal exposure is through ingestion, inhalation, and dermal contact. Accordingly, understanding the source, transport and fate of solids associated metals is a key management from a human health perspective (Filella et al. 2002, Huang and Matzner 2007, Barbieri et al. 2018, Yang et al. 2018, Mohammadi et al. 2020, Shahraki et al.2021).
Orlistat increases arsenite tolerance in THP-1 derived macrophages through the up-regulation of ABCA1
Published in Drug and Chemical Toxicology, 2022
Kaiyan Lou, Ping Huang, Huijuan Ma, Xiaolei Wang, Huan Xu, Wei Wang
Environmental arsenic exposure is a world-wide public health issue, which has been proved to be closely associated with many diseases, such as skin lesions, diabetes, cardiovascular diseases, and different types of cancers (Schuhmacher-Wolz et al. 2009, Argos et al. 2010, Ahmed et al. 2014). Our immune system is responsible for the prevention of these diseases. Arsenite (As+3), the inorganic trivalent form of arsenic, is known to induce DNA damage, cell cycle arrest, inhibition of cellular signaling and suppression of major functions in different types of immune cells (Bolt et al. 2010, Xu et al. 2016a, Soria et al. 2017). Monocytes are the important myeloid immune cells, which can be differentiated into macrophages and dendritic cells. Macrophages are professional phagocytes, which are able to digest the debris of dead cells and extrinsic pathogens (Mosser and Edwards 2008). As important innate immune cells, macrophages can also produce pro-inflammatory cytokines, such as TNF-α, IL-6, and IL-1β, superoxide, and nitric oxide (NO) to regulate the immune system (Wynn et al. 2013, Jung et al. 2018). In our previous studies, the human THP-1 monocyte cell line was differentiated into macrophages as an in vitro model to study the immunotoxicity induced by As+3 in macrophages, which demonstrated that As+3 was able to inhibit major immune functions of macrophages at nanomolar concentrations (Xu et al. 2018a).
Sodium arsenite-induced detriment of cell function in Leydig and Sertoli cells: the potential relation of oxidative damage and antioxidant defense system
Published in Drug and Chemical Toxicology, 2020
Banu Orta Yilmaz, Nebahat Yildizbayrak, Melike Erkan
TM3 Leydig and TM4 Sertoli non-tumorigenic cell lines derived from immature 11– 13-d mouse testes and were obtained from American Type Culture Collection (Manassas, VA). The cells were cultured in 1:1 mixture of Dulbecco’s modified essential medium (DMEM) and Ham’s F-12 medium with 5% horse serum, 2.5% fetal bovine serum and 1% antibiotics (Penicillin-Streptomycin-Amphotericin). Cells were maintained in a humidified atmosphere containing 95% air and 5% CO2 at 37 °C. For the exposure, sodium arsenite (CAS Number: 7784–46-5, purity ≥90%,) was dissolved in culture medium containing 1% Horse Serum and further prepared for different concentrations. In this study, 50 ppb (0.4 μM) and 1000 ppb (7.7 μM) concentrations of sodium arsenite which are approximate levels of drinking water exposure were used (Altaş et al. 2011, WHO 2011). TM3 Leydig and TM4 Sertoli cells were exposed to sodium arsenite (50 and 1000 ppb) for 24, 48, and 72 h with renewal of fresh medium containing sodium arsenite every 24 h. The control groups were treated with only culture medium containing 1% Horse Serum for each exposure time (24, 48, and 72 h).