Effect of oral methyl-t-butyl ether (MTBE) on the male mouse reproductive tract and oxidative stress in liver

Peyster, Ann de; Rodriguez, Yvonne; Shuto, Rika; Goldberg, Beck; Gonzales, Frank; Pu, Xinzhu; Klaunig, James E.

doi:10.1016/j.reprotox.2008.08.009

Cited by 17 publications

(4 citation statements)

References 20 publications

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“…15,16 Briefly, 0.2 mL serum was mixed with 40 μ L of 6 M NaOH. The mixture was incubated at 60°C for 30 minutes to hydrolyze the protein-bound MDA.…”

Section: Methodsmentioning

confidence: 99%

Oxidative Stress in Chronic Liver Disease: Relationship Between Peripheral and Hepatic Measurements

Vuppalanchi

Ghabril

Chalasani

et al. 2011

The American Journal of the Medical Sciences

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Introduction Oxidative stress plays an important role in the pathogenesis of many liver diseases. Investigators often measure markers of oxidative stress in peripheral veins as a reflection of hepatic oxidative stress as it is not always feasible to measure oxidative stress in liver tissue. However, it is unknown whether markers of oxidative stress measured from peripheral sites accurately reflect hepatic tissue oxidative stress. The aim of this study is to examine the relationship of oxidative stress marker among hepatic tissue, hepatic and peripheral veins and urine. Methods Malondialdehyde (MDA), a marker of oxidative stress was measured in hepatic vein, peripheral vein and urine samples from 26 consecutive patients undergoing transjugular liver procedures. In 19 patients undergoing liver biopsies, we measured MDA by immunohistochemical staining of paraffin-embedded liver tissue. Results Peripheral venous MDA levels showed significant correlation with hepatic venous MDA levels (r = 0.62, P = 0.02), but they did not correlate with hepatic tissue MDA content (r = 0.22, P = 0.4). Hepatic venous MDA levels did not correlate with hepatic tissue MDA content (r = −0.01, P = 0.9). Subgroup analysis of patients without portal hypertension showed a positive correlation between hepatic venous and hepatic tissue MDA levels, but this was not statistically significant (r = 0.45, P = 0.22). Urinary MDA did not correlate with MDA from any other sampling location. Conclusion Oxidative stress measured from the peripheral venous samples is poorly reflective of hepatic tissue oxidative stress. Hepatic venous sampling might be suitable for assessing hepatic tissue oxidative stress in patients without portal hypertension, but a larger study is needed to examine this possibility.

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“…15,16 Briefly, 0.2 mL serum was mixed with 40 μ L of 6 M NaOH. The mixture was incubated at 60°C for 30 minutes to hydrolyze the protein-bound MDA.…”

Section: Methodsmentioning

confidence: 99%

Oxidative Stress in Chronic Liver Disease: Relationship Between Peripheral and Hepatic Measurements

Vuppalanchi

Ghabril

Chalasani

et al. 2011

The American Journal of the Medical Sciences

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“…Malondialdehyde levels in serum and pancreatic tissue homogenates were measured using high-performance level chromatography with UV detection as described previously with some modifications. 13,14 The total antioxidant capacity in pancreatic tissue homogenates was measured using the TEAC assay described previously with some modifications. 15 …”

Section: Methodsmentioning

confidence: 99%

Effect of Different Obesogenic Diets on Pancreatic Histology in Ossabaw Miniature Swine

et al. 2011

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Objective Obesity is a factor in the outcome and severity of pancreatic conditions. We examined the effect of hypercaloric diets on the pancreata of Ossabaw swine, a large animal model of metabolic syndrome and obesity. Methods Swine were fed with 1 of 4 diets: high-fructose (n = 9), atherogenic (n = 10), modified atherogenic (n = 6), or eucaloric standard diet (n = 12) for 24 weeks. Serum chemistries were measured, and pancreata were examined for histological abnormalities including steatosis, inflammation or fibrosis, insulin content, and oxidative stress. Results The fructose, atherogenic, and modified atherogenic diet groups exhibited obesity, metabolic syndrome, islet enlargement, and significantly increased pancreatic steatosis (22.9% ± 7.5%, 19.7% ± 7.7%, and 38.7% ± 15.3% fat in total tissue area, respectively) compared with controls (9.3% ± 1.9%; P < 0.05). The modified atherogenic diet group showed significantly increased oxidative stress levels as evidenced by elevated serum malondialdehyde (3.0 ± 3.3 vs 1.5 ± 0.3 μmol/L in controls; P = 0.006) and pancreatic malondialdehyde (0.1 ± 0.12 vs 0.04 ± 0.01 nmol/mg protein in controls; P = 0.01). None of the swine exhibited pancreatitis or cellular injury. Conclusions Ossabaw swine fed with a modified atherogenic diet developed significant pancreatic steatosis and increased oxidative stress, but no other histological abnormalities were observed.

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“…10,15,16 In both animals and human, liver is the main metabolic organ of MTBE. 17,18 There are three major cytochrome P450 (CYP) enzymes involved in the metabolism of MTBE. 19,21 In animals, CYP2B1 and CYP2E1 play the most important role, while in human body CYP2A6 and CYP2E1 play the dominant role.…”

Section: Introductionmentioning

confidence: 99%

DNA polymerase β may be involved in protecting human bronchial epithelial cells from the toxic effects induced by methyl tert-butyl ether exposure

Xian

Tang

et al. 2021

Hum Exp Toxicol

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Methyl tert-butyl ether (MTBE), a widely used gasoline additive and a ubiquitous environmental pollutant in many countries and regions, can cause various kinds of toxic effects on human health. However, the molecular mechanism underlying its toxic effects remains elusive. The present study aimed to explore the cytotoxicity, DNA damage and oxidative damage effects of MTBE on human bronchial epithelial cells (16HBE) and the possible role of DNA polymerase β (pol-β) in this process. RNA interference (RNAi) was used to obtain pol-β gene knocked-down cells (pol-β−). CCK-8 assay was adopted to analyze the cell viability. Alkaline single-cell gel electrophoresis (SCGE) was performed to detect the DNA damage effects of MTBE. The enzyme activity of GSH-Px, SOD, CAT and the level of MDA were assessed. The data indicated that when treated with MTBE at the concentration exceeding 50 μmol/L and for the time exceeding 24 h, the pol-β− exhibited significantly decreased cell viability and increased DNA damage effects, as compared to the control ( P < 0.05). Furthermore, there was significant difference in the levels of GSH-pX, SOD, CAT and MDA between the pol-β− and the control ( P < 0.05). Our investigation suggests that MTBE can cause obvious cytotoxicity, DNA damage and oxidative damage effects on 16HBE cells. DNA polymerase β may be involved in protecting 16HBE cells from the toxic effects induced by MTBE exposure. These findings provide a novel insight into the molecular mechanism underlying the toxic effects of MTBE on human cells.

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Effect of oral methyl-t-butyl ether (MTBE) on the male mouse reproductive tract and oxidative stress in liver

Cited by 17 publications

References 20 publications

Oxidative Stress in Chronic Liver Disease: Relationship Between Peripheral and Hepatic Measurements

Oxidative Stress in Chronic Liver Disease: Relationship Between Peripheral and Hepatic Measurements

Effect of Different Obesogenic Diets on Pancreatic Histology in Ossabaw Miniature Swine

DNA polymerase β may be involved in protecting human bronchial epithelial cells from the toxic effects induced by methyl tert-butyl ether exposure

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