Bone Marrow Injury Induced via Oxidative Stress in Mice by Inhalation Exposure to Formaldehyde

Zhang, Yuchao; Li, Xudong; McHale, Cliona M.; Li, Rui; Zhang, Luoping; Wu, Yang; Ye, Xin; Yang, Xu; Ding, Shuzhe

doi:10.1371/journal.pone.0074974

Cited by 73 publications

(83 citation statements)

References 49 publications

(47 reference statements)

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“…Similar erythrograms were noted with quails fed 20 ml FA/kg feed (Khan et al 2005). These changes might be due to an inhibitory effect of FA on cell multiplication in bone marrow (Zhang et al 2013). Moreover, it was evident here that the FA-only-treated mice exhibited a marked rise in reticulocytes.…”

Section: Discussionsupporting

confidence: 72%

Hemato-immunologic impact of subchronic exposure to melamine and/or formaldehyde in mice

Abd‐Elhakim

Mohamed

2016

Journal of Immunotoxicology

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The aim of the present study was to explore the potential hematotoxic and immunotoxic effects of melamine (MA) in the absence and presence of formaldehyde (FA) in mice. Forty adult Swiss mice were equally allocated into four groups and daily treated with water, MA (50 mg/kg), FA (25 mg/kg), and MA þ FA respectively via feeding needle for 60 consecutive days. Hematological status was evaluated using erythrogram and leukogram profiling. Innate immune functions were assessed by measuring white blood cells lysozyme and phagocytic activities. Serum immunoglobulin levels were evaluated as indicators of humoral immunity. In addition, histologic and immunohistochemical evaluations of splenic tissues were performed. The results indicated that either MA or FA treatment resulted in significant decreases in RBCs, Hb, MCHC, total WBC, lymphocyte, and basophile levels as well as in WBCs phagocytosis and lysozyme activity. In contrast, MCV, PCV%, and reticulocyte levels were significantly increased in these hosts. The total IgM level was significantly reduced in the MA-only-exposed mice but markedly increased in the FA-only-treated ones. A significant decrease in serum IgG levels was detected following either MA or FA treatment. The combined exposure to MA and FA, compared to levels of either toxicant alone, was revealed to evoke a significant improvement in Hb, PCV%, MCV, MCHC, neutrophil, eosinophil, total IgM level, and lysozyme activity; however these values did not reach that of the controls. Furthermore, compared to control mice, both MA-only-and FA-only-treated mice showed a strong distribution of CD4 þ and CD8 þ cells in their spleens, while a moderate presence of the former cells was obvious at their co-exposure. Taken together, these findings revealed that exposure to MA or FA resulted in significant alterations in hemato-immune parameters at variable degrees while a co-exposure resulted in the mitigation of most effects of either toxicant alone. ARTICLE HISTORY

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Section: Discussionsupporting

confidence: 72%

Hemato-immunologic impact of subchronic exposure to melamine and/or formaldehyde in mice

Abd‐Elhakim

Mohamed

2016

Journal of Immunotoxicology

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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: 91%

“…[39] It causes production of oxygen radicals after entering the organism that leads to inflammation and apoptosis of most of the body cells. [40] The present study was carried out to evaluate the histological changes in the frontal cortex of the rats and the oxidative damage caused by FA and the possible protective effect of NS. Neurocytoxicity mechanisms of FA have not been revealed understood; they are assumed to be mediated by increased ROS through the activation of free radical producing enzymes and the inhibition of free radical scavenger systems.…”

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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“…Indeed, FA exposure is associated with increased ROS and the cytochrome P450 1A1 enzyme levels as well as the glutathione and the glutathione S-transferase theta 1 decreased amounts in experimental animals. 52 FA induces oxidative stress by different mechanisms, as by the inhibition of scavenger systems and the activation of oxidases. FA is a substrate for the action of the cytochrome P450 2E2 isozyme and is oxidized by peroxidase, aldehyde oxidase and xanthine oxidase with free radical production.…”

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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Bone Marrow Injury Induced via Oxidative Stress in Mice by Inhalation Exposure to Formaldehyde

Cited by 73 publications

References 49 publications

Hemato-immunologic impact of subchronic exposure to melamine and/or formaldehyde in mice

Hemato-immunologic impact of subchronic exposure to melamine and/or formaldehyde in mice

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

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

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