The disposition and intestinal absorption of zinc in rats

Yasuno, Tohru; Okamoto, Hiroki; Nagai, Miho; Kimura, Shunsuke; Yamamoto, Takanori; Nagano, Kozue; Furubayashi, Tomoyuki; Yoshikawa, Yutaka; Yasui, Hiroyuki; Katsumi, Hidemasa; Sakane, Toshiyasu; Yamamoto, Akira

doi:10.1016/j.ejps.2011.08.024

Cited by 16 publications

(10 citation statements)

References 24 publications

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“…It has been known that zinc is necessary to an optimum SOD activity since this enzyme is zinc dependent. Hence, an enhance of the stomach SOD activity could be explained by an increase in the zinc levels (Table 1), whereas no increase was observed in the intestine, since this tissue showed to absorb more zinc than the stomach (Yasuno et al, 2011). Our results are in accordance with Alvarez-Suarez et al (2011) that demonstrated a decrease in stomach SOD activity caused by oral administration of ethanol.…”

Section: Discussionsupporting

confidence: 94%

Antioxidant effect of zinc chloride against ethanol-induced gastrointestinal lesions in rats

Ineu

Oliveira

et al. 2013

Food and Chemical Toxicology

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The aim of the present study was to evaluate the possible effects of zinc chloride against the gastrointestinal lesions caused by oral administration of ethanol in rats. Rats were divided into five groups, namely, saline, ethanol, zn, zn+ethanol and ethanol+zn. Ethanol 70% (2 mL/kg) was administered by gavage in 36 h fasted rats. Zinc chloride (27 mg/kg, ~13 mg/kg of zinc) was given by gavage 1h before or 1h after the administration of ethanol. Oral administration of ethanol consistently induced damage in the rat glandular stomach and intestine. Zinc did not demonstrate effect per se and significantly reduced gastrointestinal lesions when administered either before or after lesion induction. Ethanol induced enhancement of thiobarbituric acid reactive substance and reactive species levels, diminished the ascorbic acid and total protein SH content as well as superoxide dismutase and catalase activity in stomach and intestine of rats. Zinc treatment prevented and reversed these alterations induced by ethanol. Stomach and intestine of rats treated with zinc presented higher zinc content than the tissues of rats treated only with ethanol. Non-protein SH content was not altered by any treatment. Results suggested that the gastrointestinal protective effect of zinc in this experimental model could be due to its antioxidant effect.

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Section: Discussionsupporting

confidence: 94%

Antioxidant effect of zinc chloride against ethanol-induced gastrointestinal lesions in rats

Ineu

Oliveira

et al. 2013

Food and Chemical Toxicology

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“…Moreover, net absorption is regulated by body zinc homeostasis and, thus, depend on the individual zinc status adapting to prolonged low zinc diets. Consequently, zinc-deficient humans and animals show increased fractional zinc absorption [34,[78][79][80], absorbing up to 92% of dietary zinc [34,80]. Accordingly, human zinc absorption is more efficient from low zinc diets [7].…”

Section: Zinc Absorptionmentioning

confidence: 99%

“…In the past 50 years, several analytical approaches have been applied to investigate intestinal zinc absorption and its underlying mechanisms. The latter were mainly elucidated with ex vivo animal studies, such as everted rat gut sacs [60,61], Ussing chambers with rat [225][226][227][228][229] and pig [230,231] jejunal segments, and intestinal brush-border membrane vesicles from rat [72] and pig [232,233] small intestines as well as in situ studies with isolated rat intestines using the (vascular) perfusion technique [38,70,115,234] and the intestinal loop method [79]. Moreover, some human studies using perfused intestine were performed as well [58,64].…”

Section: In Vitro Studies On Intestinal Zinc Absorptionmentioning

confidence: 99%

A Guide to Human Zinc Absorption: General Overview and Recent Advances of In Vitro Intestinal Models

2020

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Zinc absorption in the small intestine is one of the main mechanisms regulating the systemic homeostasis of this essential trace element. This review summarizes the key aspects of human zinc homeostasis and distribution. In particular, current knowledge on human intestinal zinc absorption and the influence of diet-derived factors on bioaccessibility and bioavailability as well as intrinsic luminal and basolateral factors with an impact on zinc uptake are discussed. Their investigation is increasingly performed using in vitro cellular intestinal models, which are continually being refined and keep gaining importance for studying zinc uptake and transport via the human intestinal epithelium. The vast majority of these models is based on the human intestinal cell line Caco-2 in combination with other relevant components of the intestinal epithelium, such as mucin-secreting goblet cells and in vitro digestion models, and applying improved compositions of apical and basolateral media to mimic the in vivo situation as closely as possible. Particular emphasis is placed on summarizing previous applications as well as key results of these models, comparing their results to data obtained in humans, and discussing their advantages and limitations.

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“…Evidence from animal models suggests that increased uptake of zinc by hepatocytes in the liver is the mechanism responsible. Yasuno et al [24] showed that when rats were given an intravenous dose of zinc (50 μ g/kg), the metal was rapidly distributed to the liver, spleen, intestine, kidney and pancreas. Moreover, systemic inflammation in mice resulted in IL-6-dependent up-regulation of the zinc importer Slc39a14 , which enabled zinc uptake by hepatocytes in the liver [25,26].…”

Section: Introductionmentioning

confidence: 99%

Metal ions in macrophage antimicrobial pathways: emerging roles for zinc and copper

et al. 2013

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The immunomodulatory and antimicrobial properties of zinc and copper have long been appreciated. In addition, these metal ions are also essential for microbial growth and survival. This presents opportunities for the host to either harness their antimicrobial properties or limit their availability as defence strategies. Recent studies have shed some light on mechanisms by which copper and zinc regulation contribute to host defence, but there remain many unanswered questions at the cellular and molecular levels. Here we review the roles of these two metal ions in providing protection against infectious diseases in vivo, and in regulating innate immune responses. In particular, we focus on studies implicating zinc and copper in macrophage antimicrobial pathways, as well as the specific host genes encoding zinc transporters (SLC30A, SLC39A family members) and CTRs (copper transporters, ATP7 family members) that may contribute to pathogen control by these cells.

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The disposition and intestinal absorption of zinc in rats

Cited by 16 publications

References 24 publications

Antioxidant effect of zinc chloride against ethanol-induced gastrointestinal lesions in rats

Antioxidant effect of zinc chloride against ethanol-induced gastrointestinal lesions in rats

A Guide to Human Zinc Absorption: General Overview and Recent Advances of In Vitro Intestinal Models

Metal ions in macrophage antimicrobial pathways: emerging roles for zinc and copper

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