In vitro effect of methanol on folate-deficient rat hepatocytes

Datta, Nita Jang; Namasivayam, A

doi:10.1016/s0376-8716(03)00066-8

Cited by 24 publications

(19 citation statements)

References 17 publications

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“…54 Impaired antioxidant enzyme activities in the metabolic detoxification of oxidative by-products were also associated with in vivo FA treatments. 53,55 FA exposure also leads to inflammation and to a consequent excess of ROS. 31,56 ROS, as hydrogen peroxide and hypochlorite acid, are indeed generated from the oxidative burst of activated alveolar macrophages and neutrophils.…”

Section: Discussionmentioning

confidence: 99%

Formaldehyde-induced toxicity in the nasal epithelia of workers of a plastic laminate plant

et al. 2016

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Formaldehyde is a ubiquitous volatile organic compound widely used for various industrial purposes. Formaldehyde was reclassified by the International Agency for Research on Cancer as a human carcinogen, based on sufficient evidence for a casual role for nasopharyngeal cancer. However, the mechanisms by which this compound causes nasopharyngeal cancer are not completely understood. Therefore, we have examined the formaldehyde-induced toxicity in the nasal epithelia of the workers of a plastic laminate plant in Bra, Cuneo, Piedmont region, North-Western Italy, hence in the target site for formaldehyderelated nasal carcinogenesis. We have conducted a cross-sectional study aimed at comparing the frequency of 3-(2-deoxy-β-D-erythro-pentafuranosyl)pyrimido[1,2-α]purin-10(3H)-one deoxyguanosine (M 1 dG) adducts, a biomarker of oxidative stress and lipid peroxidation, in 50 male exposed workers and 45 male controls using 32 P-DNA post-labeling. The personal levels of formaldehyde exposure were analysed by gas-chromatography mass-spectrometry. The smoking status was estimated by measuring the concentrations of urinary cotinine by gas-chromatography mass-spectrometry. The air monitoring results showed that the exposure levels of formaldehyde were significantly greater for the plastic laminate plant workers, 211.4 ± 14.8 standard error (SE) µg m −3 , than controls, 35.2 ± 3.4 (SE) µg m −3 , P < 0.001. The levels of urinary cotinine were 1064 ± 118 ng ml −1 and 14.18 ± 2.5 ng ml −1 in smokers and non-smokers, respectively, P < 0.001. The M 1 dG adduct frequency per 10 8 normal nucleotides was significantly higher among the workers of the plastic laminate plant exposed to formaldehyde, 111.6 ± 14.3 (SE), compared to controls, 49.6 ± 3.4 (SE), P < 0.001. This significant association persisted also when personal dosimeters were used to measure the extent of indoor levels of formaldehyde exposure. No influences of smoking and age were observed across the study population. However, after categorization for occupational exposure, a significant effect was found in the controls, P = 0.018, where the levels of DNA damage were significantly correlated with the levels of urinary cotinine, regression coefficient (β) = 0.494 ± 0.000 (SE), P < 0.002. Our findings indicated that M 1 dG adducts constitute a potential mechanism of formaldehydeinduced toxicity. Persistent DNA damage contributes to the general decline of the physiological mechanisms designed to maintain cellular homeostasis.

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Section: Discussionmentioning

confidence: 99%

Formaldehyde-induced toxicity in the nasal epithelia of workers of a plastic laminate plant

et al. 2016

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“…[33] Datta and Namasivayam [42] and Farooqui et al [43] suggested that FA exposure in experimental animals has a negative impact on the antioxidant system; impaired antioxidant enzyme activity causes ROS-induced membrane lipid and protein oxidation leading to delayed apoptotic/necrotic cell death. [40,[42][43][44] The current study revealed a significant increase in the levels of LPO in the brain tissue in FA-treated rats compared to the control group. Similar findings were observed in rats treated with lead acetate.…”

Section: Discussionmentioning

confidence: 99%

Nigella sativa protects against formaldehyde-induced neurotoxicity in the rat frontal cortex

Mohamad¹,

Essa²,

Ata³

2015

Anatomy

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Formaldehyde (FA) is a compound commonly used in industry and medicine that can react with different macromolecules such as proteins, nucleic acids and low molecular weight substances as amino acids. [1,2] In particular, anatomists and medical students are exposed to FA gas during cadaver dissections. [3,4] Humans are exposed to FA from direct environmental sources like paint, plywood, cosmetics, cigarette smoke, photochemical smog and even various fruits as well as from the metabolism of xenobiotics. [5,6] FA is accepted as toxic over certain doses and its at high room temperatures its harmful effects increase due to volatility. [7][8][9][10] Physiological FA forms by the metabolism of L-methionine, histamine or methylamine in the body, and contribute to biological methylation by folic acid. [11] Acute exposure to FA causes central nervous system symptoms such as headache, malaise, insomnia, anorexia

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“…18,28) Previous studies have reported that the FA suppressed SOD activities. 16,29,30) In this study, we observed that SOD and GSH levels decreased while MDA levels significantly increased, which revealed a higher lipid per- oxidation after FA exposure, and Vit E reversed these alternation; an in vitro experiment confirmed Vit E could reverse FA induced cell apoptosis.…”

Section: Discussionmentioning

confidence: 99%

“…16,17) In the cardiovascular system, ROS are implicated in the pathogenesis of atherosclerosis, reperfusion injury, hypertension, and heart failure, as increase oxidative stress induced apoptosis and necrosis of myocytes. 18) Overproduction of ROS, or low levels of available antioxidants, can cause Wu, ET AL DNA, proteins, and lipids damage, which implies that ROS overload during pregnancy may induce developmental toxicity and result in defects in many tissues, such as myocytes in the offspring. FA exposure can increase ROS in many tissues.…”

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confidence: 99%

Vitamin E Reversed Apoptosis of Cardiomyocytes Induced by Exposure to High Dose Formaldehyde During Mice Pregnancy

Jiang

Gong

et al. 2017

Int. Heart J.

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SummaryIn this study, we investigated the protection effect of Vitamin E (Vit E) on formaldehyde (FA) exposure during pregnancy induced apoptosis of cardiomyocytes, and used an HL-1 cell line to confirmed the findings in vivo.Pregnant mice received different doses of FA (0.5 mg/kg, 1.0 mg/kg, 1.5 mg/kg, 0.1 μg Vit E, or 1.5 mg/ kg + 0.1 μg Vit E). TUNEL staining was used to reveal the apoptosis in cardiomyocytes, and SOD, MDA, GSH, Livin, and Caspase-3 in cardiomyocytes were detected by ELISA, RT-PCR, and Western blot. For in vitro study, HL-1 cells were treated with vehicle, 5 μmol/L FA, 25 μmol/L FA, 50 μmol/L FA, 10 mg/L Vit. E, and 50 μmol/L FA+ 10 mg/L Vit E, respectively. CCK-8 assay and flow cytometry were used to evaluate cell vitality and apoptosis. A high dose of FA exposure led to cytotoxicity in both pregnant mice and offspring, as TUNEL staining revealed a significant apoptosis of cardiomyocytes, and the alternation in SOD, GSH, MDA, Livin, and Caspase-3 was found in cardiomyocytes. 0.1 μg Vit. E could reverse high doses of FA exposure induced apoptosis of cardiomyocytes in both pregnant mice and offspring. The in vitro study revealed that FA exposure induced a decrease of cell viability and increased cell apoptosis, as well as oxidative stress in HL-1 cells with alternation in SOD, GSH, MDA, Livin, and Caspase-3.This study revealed a high dose of FA induced oxidative stress and apoptosis of cardiomyocytes in both pregnant mice and offspring, and Vit E supplement during pregnancy reversed the systemic and myocardial toxicity of FA.(Int Heart J 2017; 58: 769-777)

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In vitro effect of methanol on folate-deficient rat hepatocytes

Cited by 24 publications

References 17 publications

Formaldehyde-induced toxicity in the nasal epithelia of workers of a plastic laminate plant

Formaldehyde-induced toxicity in the nasal epithelia of workers of a plastic laminate plant

Nigella sativa protects against formaldehyde-induced neurotoxicity in the rat frontal cortex

Vitamin E Reversed Apoptosis of Cardiomyocytes Induced by Exposure to High Dose Formaldehyde During Mice Pregnancy

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