Effects of methyl mercury on the activity and gene expression of mouse Langerhans islets and glucose metabolism

Maqbool, Faheem; Bahadar, Haji; Niaz, Kamal; Baeeri, Maryam; Rahimifard, Mahban; Navaei-Nigjeh, Mona; Ghasemi-Niri, Seyedeh Farnaz; Abdollahi, Mohammad

doi:10.1016/j.fct.2016.05.005

Cited by 33 publications

(19 citation statements)

References 49 publications

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“…MeHg exposure inhibits paraoxonase-1, which prevents the atherosclerotic process by metabolizing toxic oxidized lipids associated with LDL and HDL [ 30 ]. Therefore, Hg induces oxidative stress and disrupts gluconeogenesis, resulting in systemic inflammation that affects the accumulation of abnormal adipocytes [ 23 , 31 ]. Our results showed that the levels of blood Hg were significantly higher ( p <.0001) in the hyperlipidemia group (male: 4.03 μg/L, female: 2.83 μg/L) than in the non-hyperlipidemia group (male: 3.48 μg/L, female: 2.69 μg/L), and that an increase of 1 μg/L blood Hg was associated with an 11% increase in the odds of hyperlipidemia, even after adjustment for personal medications.…”

Section: Discussionmentioning

confidence: 99%

Mercury Exposure and Associations with Hyperlipidemia and Elevated Liver Enzymes: A Nationwide Cross-Sectional Survey

Lee

Cho

Jeong

et al. 2020

Toxics

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Mercury (Hg) has obesogenic properties. However, the associated health outcomes of population-level mercury exposure were unclear. This study investigated the relationships between blood mercury levels and obesity-related outcomes such as hyperlipidemia and elevated liver enzymes. Using the second cycle of the Korean National Environmental Health Survey (n = 6454), we performed logistic regression to examine the effects of Hg on hyperlipidemia and elevated liver enzymes. The blood mercury levels were significantly higher in the hyperlipidemia group (n = 3699, male: 4.03 μg/L, female: 2.83 μg/L) compared to the non-hyperlipidemia group (n = 2755, male: 3.48 μg/L, female: 2.69 μg/L), and high blood mercury levels were associated with an 11% higher risk of hyperlipidemia. The elevated liver enzymes group had higher mean blood mercury levels (n = 1189, male: 4.38 μg/L, female: 3.25 μg/L) than the normal group (n = 5265, male: 3.64 μg/L, female: 2.70 μg/L), and elevated blood mercury was associated with a 35% higher risk of elevated liver enzymes. Moreover, the effect was constant after adjusting for personal medications. These results indicate that mercury exposure is significantly associated with hyperlipidemia and elevated liver enzymes.

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Section: Discussionmentioning

confidence: 99%

Mercury Exposure and Associations with Hyperlipidemia and Elevated Liver Enzymes: A Nationwide Cross-Sectional Survey

Lee

Cho

Jeong

et al. 2020

Toxics

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“…Ferrous reducing antioxidant power (FRAP) assay is an indication of the antioxidant power of the biological samples. The protocol was used previously described by Maqbool et al Total antioxidant power (TAP) was determined by measuring the ability to reduce Fe 3+ to Fe 2+ . The following procedure leads to the preparation of the FRAP reagent: mixing of acetate buffer 300 mM pH 3.6; TPTZ: 10 mM in 40 mM HCl; and FeCl 3 .6H 2 O: 20 mM, in the ratio of 10:1:1 just before testing.…”

Section: Methodsmentioning

confidence: 99%

Molecular mechanisms of action of styrene toxicity in blood plasma and liver

Niaz

Mabqool

Khan

et al. 2017

Environmental Toxicology

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Styrene is an aromatic colorless hydrocarbon available in liquid form and highly volatile. In its pure form, it gives a sweet smell. The primary source of exposure in the environment is from plastic materials, rubber industries, packaging materials, insulations, and fiber glass and carpet industry. Natural sources of styrene include: few metabolites in plants which are transferred through food chain. The current study was designed to evaluate styrene toxicity, including: superoxide dismutase (SOD) and protein carbonyl, oxidative stress, glucose-6-phosphatase (G6Pase), glycogen phosphorylase (GP), and phosphoenolpyruvate carboxykinase (PEPCK) activities, adenosine triphosphate (ATP) to adenosine diphosphate (ADP) ratio, and changes in gene expressions such as glutamate dehydrogenase 1 (GLUD1), glucose transporter 2 (GLUT2), and glucokinase (GCK) in the rat liver tissue. For this purpose, styrene was dissolved in corn oil and was administered via gavage, at doses 250, 500, 1000, 1500, 2000, mg/kg/day per mL and control (corn oil) to each rat with one day off in a week, for 42 days. Plasma SOD and protein carbonyl of plasma were significantly up-regulated in 1000, 1500, and 2000 mg/kg/day styrene administrated groups (P < .001). In addition, styrene caused an increase in lipid peroxidation (LPO) and reactive oxygen species (ROS) in the dose-dependent manners in liver tissue (P < .001). Furthermore, the ferrous reducing antioxidant power (FRAP) and total thiol molecules (TTM) in styrene-treated groups were significantly decreased in liver tissue (P < .001) with increasing doses. In treated rats, styrene significantly increased G6Pase activity (P < .001) and down-regulated GP activity (P < .001) as compared to the control group. The PEPCK activity was significantly raised in a dose-dependent manner (P < .001). The ATP/ADP ratio of live cells was significantly raised by increasing the dose (P < .001). There was significantly an up-regulation of GLUD1 and GCK at 2000 mg/kg group (P < .01) and a down-regulation for GLUT2 at the same dose. While in the rest of group, GLUT2 showed up-regulation of relative fold change. By targeting genes such as GLUD1, GLUT2, and GCK, disruption of hepatic gluconeogenesis, glycogenolysis, and insulin secretory functions are obvious. The present study illustrates that induction of oxidative stress followed by changes in G6Pase, GP, and PEPCK activities and the genes responsible for glucose metabolism are the mechanisms of styrene's action in the liver.

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“…Through RNA sequencing of exposed zebrafish embryos, another study further suggests that binding of MeHg to selenocysteine blocks the availability of selenium and results in altered intracellular redox states [200]. In postnatal animal studies, juvenile mice chronically exposed for 2–6 weeks with MeHgCl had significantly altered glucose-insulin homeostasis, increased ROS in pancreatic islets, and reduced antioxidant-related defenses [201, 202]. Progressively higher levels of ROS generation in the juvenile mouse pancreas led to lipid peroxidation in plasma and islets [201].…”

Section: Developmental Disruptions Resulting From Chemical-inducedmentioning

confidence: 99%

Redox stress and signaling during vertebrate embryonic development: Regulation and responses

Timme‐Laragy

Hahn

Hansen

et al. 2018

Seminars in Cell & Developmental Biology

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Vertebrate embryonic development requires specific signaling events that regulate cell proliferation and differentiation to occur at the correct place and the correct time in order to build a healthy embryo. Signaling pathways are sensitive to perturbations of the endogenous redox state, and are also susceptible to modulation by reactive species and antioxidant defenses, contributing to a spectrum of passive vs. active effects that can affect redox signaling and redox stress. Here we take a multi-level, integrative approach to discuss the importance of redox status for vertebrate developmental signaling pathways and cell fate decisions, with a focus on glutathione/glutathione disulfide, thioredoxin, and cysteine/cystine redox potentials and the implications for protein function in development. We present a tissue-specific example of the important role that reactive species play in pancreatic development and metabolic regulation. We discuss NFE2L2 (also known as NRF2) and related proteins, their roles in redox signaling, and their regulation of glutathione during development. Finally, we provide examples of xenobiotic compounds that disrupt redox signaling in the context of vertebrate embryonic development. Collectively, this review provides a systems-level perspective on the innate and inducible antioxidant defenses, as well as their roles in maintaining redox balance during chemical exposures that occur in critical windows of development.

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Effects of methyl mercury on the activity and gene expression of mouse Langerhans islets and glucose metabolism

Cited by 33 publications

References 49 publications

Mercury Exposure and Associations with Hyperlipidemia and Elevated Liver Enzymes: A Nationwide Cross-Sectional Survey

Mercury Exposure and Associations with Hyperlipidemia and Elevated Liver Enzymes: A Nationwide Cross-Sectional Survey

Molecular mechanisms of action of styrene toxicity in blood plasma and liver

Redox stress and signaling during vertebrate embryonic development: Regulation and responses

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