N,N’ bis-(2-mercaptoethyl) isophthalamide induces developmental delay in Caenorhabditis elegans by promoting DAF-16 nuclear localization

Tao, Ke; Soares, Félix Alexandre Antunes; Santamarı́a, Abel; Bowman, Aaron B.; Skalny, Anatoly V.; Aschner, Michael

doi:10.1016/j.toxrep.2020.07.012

Cited by 9 publications

(1 citation statement)

References 34 publications

(53 reference statements)

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“…The results showed that 12.5 and 25 μM ACR exposure decreased the cytosolic localization of DAF-16 (decreased to 22.2% and 7.8%), suggesting that the low concentration of ACR activated the antioxidant resistance caused by DAF-16/FOXO ( Figure 7 ). It was consistent with the findings that exposure to pharmaceuticals which induce oxidative stress, such as H 2 O 2 , N , N ′ bis-(2-mercaptoethyl) isophthalamide, juglone, and so on, could lead to the DAF-16 nuclear translocation [ 38 , 39 , 40 ]. It is worth noting that, with high exposure to ACR, the percentages of DAF-16 nuclear localization were decreased significantly (50 μM, 43.8%; 100 μM, 16.0%) ( p < 0.01) as compared to those treated with 25 μM of ACR, and this is similar to what was found in chronic exposure of zearalenone [ 41 ].…”

Section: Resultssupporting

confidence: 89%

Acrolein Promotes Aging and Oxidative Stress via the Stress Response Factor DAF-16/FOXO in Caenorhabditis elegans

Song

Xie

et al. 2022

Foods

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For this investigation, Caenorhabditis elegans (C. elegans) served, for the first time, as a model organism to evaluate the toxic effect and possible underlying mechanisms under acrolein (ACR) exposure. The results showed that ACR exposure (12.5–100 μM) shortened the lifespan of C. elegans. The reproductive capacity, body length, body width, and locomotive behavior (head thrash) of C. elegans were diminished by ACR, especially the doses of 50 and 100 μM. Furthermore, ACR significantly enhanced the endogenous ROS levels of C. elegans, inhibited the antioxidant-related enzyme activities, and affected the expression of antioxidant related genes. The increasing oxidative stress level promoted the migration of DAF-16 into the nucleus that was related to the DAF-16/FOXO pathway. It was also confirmed by the significant decrease of the lifespan-shortening trend in the daf-16 knockout mutant. In conclusion, ACR exposure induced aging and oxidative stress in C.elegans, resulting in aging-related decline and defense-related DAF-16/FOXO pathways’ activation.

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Section: Resultssupporting

confidence: 89%

Acrolein Promotes Aging and Oxidative Stress via the Stress Response Factor DAF-16/FOXO in Caenorhabditis elegans

Song

Xie

et al. 2022

Foods

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Reductions in plasma and urine mercury concentrations following N,N′bis-(2-mercaptoethyl) isophthalamide (NBMI) therapy: a post hoc analysis of data from a randomized human clinical trial

Geier,

Geier

2023

Biometals

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Environmental mercury exposure possesses a significant risk to many human populations. At present there are no effective treatments for acute mercury toxicity. A new compound, N,N′bis-(2-mercaptoethyl) isophthalamide (NBMI), a lipophilic chelating agent was created to tightly/irreversibly bind mercury. A post hoc dose-dependent analysis of NBMI therapy was undertaken on data from a randomized controlled NBMI human treatment trial on 36 Ecuadorian gold miners with elevated urinary mercury concentrations. Study subjects were randomly assigned to receive 100 milligram (mg) NBMI/day, 300 mg NBMI/day, or placebo for 14 days. For each study subject daily mg NBMI dose/Kilogram (Kg) bodyweight were determined and plasma and urine mercury concentrations (micrograms (µg)/Liter (L)) on study day 1 (pre-NBMI treatment), 15 (after 14 days of NBMI treatment) and 45 (30 days after NBMI treatment) were correlated with NBMI dosing using the linear regression statistic in SAS. Regression revealed significant inverse correlations between increasing per mg NBMI/Kg bodyweight/day and reduced concentrations of urinary and plasma mercury on study day 15 (reduced by in urine = 18–20 µg/L and plasma = 2 µg/L) and study day 30 (reduced by in urine = 15–20 µg/L and plasma = 4 µg/L) and significant correlations between reductions in mercury concentrations in urine and plasma. Significant 30% reductions in urinary mercury concentrations per mg NBMI/Kg bodyweight/day administered for 14 days were observed. This study supports the dose-dependent ability of NBMI therapy to significantly reduce mercury concentrations, particularly in the urine, in an acutely mercury exposed human population. NBMI therapy should be evaluated in other mercury exposed populations.

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The Role of Human LRRK2 in Acute Methylmercury Toxicity in Caenorhabditis elegans

Rocha

Tinkov

et al. 2021

Neurochem Res

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N,N’ bis-(2-mercaptoethyl) isophthalamide induces developmental delay in Caenorhabditis elegans by promoting DAF-16 nuclear localization

Abstract: Graphical abstract

Cited by 9 publications

References 34 publications

Acrolein Promotes Aging and Oxidative Stress via the Stress Response Factor DAF-16/FOXO in Caenorhabditis elegans

Acrolein Promotes Aging and Oxidative Stress via the Stress Response Factor DAF-16/FOXO in Caenorhabditis elegans

Reductions in plasma and urine mercury concentrations following N,N′bis-(2-mercaptoethyl) isophthalamide (NBMI) therapy: a post hoc analysis of data from a randomized human clinical trial

The Role of Human LRRK2 in Acute Methylmercury Toxicity in Caenorhabditis elegans

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