Gastrointestinal absorption of inorganic mercuric compounds in vivo and in situ

Endo, Tokiko; Nakaya, Shozo; Kimura, Ryohei; Murata, Toshiro

doi:10.1016/0041-008x(84)90146-7

Cited by 29 publications

(34 citation statements)

References 9 publications

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“…Subsequent co-administration of bile and HgCl 2 increased the absorption of Hg 2+ in the duodenum to levels similar to those observed in control rats. Furthermore, it was shown that the accumulation of Hg 2+ in the cells of the small intestine was greatest when the pH of the perfusion solution was 4.7 (Endo et al, 1984(Endo et al, , 1986. In contrast, when the pH of the perfusion solution was 8.0, the accumulation of Hg 2+ in the intestine was significantly lower than that at pH 4.7.…”

Section: Molecular Mimicry and The Intestinal Transport Of Hg 2+mentioning

confidence: 94%

“…In vivo studies, in which sections of rat duodenum, jejunum, ileum and stomach were perfused with HgCl 2 for various time intervals, demonstrated that the duodenum is the primary site of Hg 2+ absorption within the gastrointestinal tract of rats (Endo et al, 1984). Interestingly, in rats with ligated bile ducts, the absorption of Hg 2+ was decreased significantly.…”

Section: Molecular Mimicry and The Intestinal Transport Of Hg 2+mentioning

confidence: 99%

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Molecular and ionic mimicry and the transport of toxic metals

Bridges

Zalups

2005

Toxicology and Applied Pharmacology

677

460

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Despite many scientific advances, human exposure to, and intoxication by, toxic metal species continues to occur. Surprisingly, little is understood about the mechanisms by which certain metals and metal-containing species gain entry into target cells. Since there do not appear to be transporters designed specifically for the entry of most toxic metal species into mammalian cells, it has been postulated that some of these metals gain entry into target cells, through the mechanisms of ionic and/or molecular mimicry, at the site of transporters of essential elements and/or molecules. The primary purpose of this review is to discuss the transport of selective toxic metals in target organs and provide evidence supporting a role of ionic and/or molecular mimicry. In the context of this review, molecular mimicry refers to the ability of a metal ion to bond to an endogenous organic molecule to form an organic metal species that acts as a functional or structural mimic of essential molecules at the sites of transporters of those molecules. Ionic mimicry refers to the ability of a cationic form of a toxic metal to mimic an essential element or cationic species of an element at the site of a transporter of that element. Molecular and ionic mimics can also be sub-classified as structural or functional mimics. This review will present the established and putative roles of molecular and ionic mimicry in the transport of mercury, cadmium, lead, arsenic, selenium, and selected oxyanions in target organs and tissues.

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Section: Molecular Mimicry and The Intestinal Transport Of Hg 2+mentioning

confidence: 94%

Section: Molecular Mimicry and The Intestinal Transport Of Hg 2+mentioning

confidence: 99%

Molecular and ionic mimicry and the transport of toxic metals

Bridges

Zalups

2005

Toxicology and Applied Pharmacology

677

460

View full text Add to dashboard Cite

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“…Owing to these similarities and because amino acid and peptide transporters are prevalent in enterocytes (Dave et al 2004; Ganapathy et al 2001), it is possible that thiol S -conjugates of Hg 2+ are taken up into enterocytes by one or more of amino acid and/or peptide transporters. The duodenum, which is a major site of amino acid absorption, also appears to be the initial site of Hg 2+ absorption (Endo et al 1984). This observation supports the theory that amino acid and/or peptide transporters may be involved in the intestinal uptake of mercuric species.…”

Section: Transport Of Inorganic Mercurymentioning

confidence: 99%

Mechanisms involved in the transport of mercuric ions in target tissues

2016

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Mercury exists in the environment in various forms, all of which pose a risk to human health. Despite guidelines regulating the industrial release of mercury into the environment, humans continue to be exposed regularly to various forms of this metal via inhalation or ingestion. Following exposure, mercuric ions are taken up by and accumulate in numerous organs, including brain, intestine, kidney, liver, and placenta. In order to understand the toxicological effects of exposure to mercury, a thorough understanding of the mechanisms that facilitate entry of mercuric ions into target cells must first be obtained. A number of mechanisms for the transport of mercuric ions into target cells and organs have been proposed in recent years. However, the ability of these mechanisms to transport mercuric ions and the regulatory features of these carriers have not been characterized completely. The purpose of this review is to summarize the current findings related to the mechanisms that may be involved in the transport of inorganic and organic forms of mercury in target tissues and organs. This review will describe mechanisms known to be involved in the transport of mercury and will also propose additional mechanisms that may potentially be involved in the transport of mercuric ions into target cells.

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“…Presenting complaints following ingestion may include nausea, vomiting, abdominal pain, or hematemesis. Colitis with necrosis or mucosal sloughing may occur in severe cases, leading to excessive volume loss [56,88,89].…”

Section: De Rusyniak Et Al 374mentioning

confidence: 99%

Heavy metal poisoning: management of intoxication and antidotes

Rusyniak

Arroyo

Acciani

et al. 2010

Experientia Supplementum

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Abstract. Of the known elements, nearly 80% are either metals or metalloids. The highly reactive nature of most metals result in their forming complexes with other compounds such oxygen, sulfide and chloride. Although this reactivity is the primary means by which they are toxic, many metals, in trace amounts, are vital to normal physiological processes; examples include iron in oxygen transport, manganese and selenium in antioxidant defense and zinc in metabolism. With these essential metals toxicity occurs when concentrations are either too low or too high. For some metals there are no physiological concentrations that are beneficial; as such these metals only have the potential to cause toxicity. This chapter focuses on four of these: arsenic, mercury, lead and thallium.

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Gastrointestinal absorption of inorganic mercuric compounds in vivo and in situ

Cited by 29 publications

References 9 publications

Molecular and ionic mimicry and the transport of toxic metals

Molecular and ionic mimicry and the transport of toxic metals

Mechanisms involved in the transport of mercuric ions in target tissues

Heavy metal poisoning: management of intoxication and antidotes

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