Oral exposure of Kunming mice to diisononyl phthalate induces hepatic and renal tissue injury through the accumulation of ROS. Protective effect of melatonin

Ma, Ping; Yan, Biao; Zeng, Qiang; Liu, Xudong; Wu, Yang; Jiao, Ming; Liu, Chao; Wu, Jiliang; Yang, Xu

doi:10.1016/j.fct.2014.03.027

Cited by 73 publications

(53 citation statements)

References 64 publications

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“…Similarly, a decrease in GSH was observed with the simultaneous increase in ROS level. These phenomena may be explained by the fact that increased exposure times inevitably lead to cell death and that intracellular oxidative damage promotes an imbalance in ROS and GSH levels (Ma et al, 2014). Figure 6 shows that MDA levels are higher in cells treated for 48 h than in cells treated for only 24 h. This trend directly contrasts observed ROS and GSH levels, which continued to increase with exposure time.…”

Section: Discussionmentioning

confidence: 58%

“…When produced in excess, ROS can cause tissue injury. Tissue injury itself can cause ROS generation (Ma et al, 2014). Research results show that ROS generation during the oxidation process is an important cause of biological toxicity of nanomaterials (Nel et al, 2006) and that nanoparticles can also generate ROS (Kim et al, 2010).…”

Section: Discussionmentioning

confidence: 96%

“…ROS levels were measured by monitoring increases in the fluorescence intensity of DCF using a previously described procedure with minor modifications according to the method of Ma et al (2014).…”

Section: Intracellular Ros Generation Assaymentioning

confidence: 99%

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Comparative study of oxidative stress induced by sand flower and schistose nanosized layered double hydroxides in N2a cells

Yan

et al. 2015

Front. Biol.

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Magnesium-aluminum layered double hydroxide (Mg/Al-LDH) nanoparticles have strong potential application as drug delivery systems because of their low toxicity and suitable biocompatibility. However, few studies have described the morphological effects of these hydroxides on nerve cells. The present study compares the oxidative stress induced by different concentrations (i.e., 0, 50, 100, 200, 400, and 800 μg/mL) of sand flower and flake nano-Mg/ Al-LDHs in mouse neuroblastoma cells (N2a) when these cells were exposed for 24 and 48 h. Cell viability was detected by MTT assay, and production of reactive oxygen species (ROS), glutathione (GSH), and malondialdehyde (MDA) were monitored to evaluate oxidative damage. Results suggested that sand flower nano-LDHs, at the appropriate concentrations (less than 200 μg/mL), especially those of about 100-200 nm in size, induce no harmful effects on N2a cells.

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Section: Discussionmentioning

confidence: 58%

Section: Discussionmentioning

confidence: 96%

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Comparative study of oxidative stress induced by sand flower and schistose nanosized layered double hydroxides in N2a cells

Yan

et al. 2015

Front. Biol.

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“…Diisononyl phthalates (DINP), a relatively new type of plasticizer, are added to cosmetics as vehicles for fragrance, and to plastics to make them soft and flexible, such as in children's toys and medical devices (Ma et al, 2014). DINP makes up approximately 30 percent of all plasticizers used worldwide.…”

Section: Introductionmentioning

confidence: 99%

Long-term dermal exposure to diisononyl phthalate exacerbates atopic dermatitis through oxidative stress in an FITC-induced mouse model

et al. 2015

Front. Biol.

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Diisononyl phthalate (DINP), considered to be an environmentally friendly plasticizer, is now widely used. However, the toxic effects of DINP need to be examined, particularly the effects of long-term dermal DINP exposure. Research into the mechanisms underlying these effects is urgently needed. In this study we examined the exacerbation effect of long-term dermal exposure to DINP in fluorescein isothiocyanate (FITC)-induced contact hypersensitivity (CHS) in mice, and sought the potential molecular mechanisms. Forty-nine male Balb/c mice were subjected to a 40-day dermal exposure to saline or one of three concentrations of DINP and then three rounds of sensitization with vehicle or 0.5% FITC. The results of a histopathological examination and measurement of ear swelling as well as immunological and inflammatory biomarkers (total-immunoglobulin (Ig)E and Th cytokines) supported the notion that high doses of DINP may aggravate atopic dermatitis. We also showed that melatonin, an antioxidant, could decrease the levels of oxidative stress and alleviate FITC-induced CHS suggesting that oxidative stress may be one of the molecular mechanisms to explain the exacerbation effect induced by DINP.

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“…The direct scavenging actions of melatonin as well as its indirect effects on the enzymes which inhibit the synthesis and/or detoxify the oxidative stress inducers such as hydroxyl radical, hydrogen peroxide, peroxynitrite anion, nitric oxide and hypochlorous acid are induced with both physiological and pharmacological levels of melatonin (Reiter et al, 1995;1997;Kolli et al, 2013;Ma et al, 2014).…”

Section: Introductionmentioning

confidence: 99%

Influence of subacute melatonin treatment on antioxidant factors in the liver of female rats

Abdallah

Karacaoğlu

Girgin

et al. 2015

J. Exper. Appl. Anim. Sci.

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Melatonin is a well-known antioxidant substance. The attention paid to its adverse effects is limited. Moreover, data published about its toxicity and /or undesired effects are scarce in the literature. The main aim of the present study was to evaluate subacute melatonin effects on antioxidant enzymes, lipid peroxidation and liver transferases in experimental animals. FemaleWistar rats were used in this study and divided into two groups. Group I was a control group and received corn oil. Group II was treated with 100 mg/kg (oral) melatonin for 7 days. The antioxidant enzyme activities such as superoxide dismutase (SOD), catalase (CAT) and lipid peroxidation marker malondialdehyde (MDA) levels were measured. Alanine aminotransferase (ALT), aspartate aminotransferase (AST), alkaline phosphatase (ALP), cholesterol and urea levels were also measured. Additionally, histopathological evaluations of hepatic tissue samples were performed. The obtained results showed that the subacute melatonin exposure reduced both antioxidant CAT activity and MDA levels (both, p<0.05). However, ALT and AST levels increased in melatonin treated rats (both, p<0.05). The ratio of AST to ALT in the melatonin treated group was nearly two-fold higher than the control group. Microscopic examination revealed no severe histopathological changes in the liver. In conclusion, melatonin treatment causes changes in female rats liver functions and further investigations are necessary to examine the full impact of melatonin supplementation with regards to route of administration, dose as well as the exposure period.

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Oral exposure of Kunming mice to diisononyl phthalate induces hepatic and renal tissue injury through the accumulation of ROS. Protective effect of melatonin

Cited by 73 publications

References 64 publications

Comparative study of oxidative stress induced by sand flower and schistose nanosized layered double hydroxides in N2a cells

Comparative study of oxidative stress induced by sand flower and schistose nanosized layered double hydroxides in N2a cells

Long-term dermal exposure to diisononyl phthalate exacerbates atopic dermatitis through oxidative stress in an FITC-induced mouse model

Influence of subacute melatonin treatment on antioxidant factors in the liver of female rats

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