Cell death pathways of particulate matter toxicity

Peixoto, Milena Simões; Galvão, Marcos Felipe de Oliveira; Medeiros, Sílvia Regina Batistuzzo de

doi:10.1016/j.chemosphere.2017.08.076

Cited by 132 publications

(87 citation statements)

References 203 publications

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“…However, its peel and seeds are discarded by frozen pulp companies, generating a large quantity of byproduct. The consumption of camu-camu pulp is related to its unique taste and high ascorbic acid content, but recently chemical and functional analyses of camu-camu byproducts have indicated in vitro and in vivo functional properties, such as antioxidant, antihyperglycemic, antihyperlipidemic, antihypertensive, antimicrobial, and neuroprotective effects (de Souza Schmidt Gonçalves et al, 2014;Azevêdo et al, 2015;Fujita et al, 2015;Miyashita et al, 2017;Fidelis et al, 2018). Camu-camu byproducts have the potential to be used in developing new bioactive-rich foods and possibly eliminating the use of synthetic chemical preservatives in processed foods.…”

Section: Introductionmentioning

confidence: 99%

From byproduct to a functional ingredient: Camu-camu (Myrciaria dubia) seed extract as an antioxidant agent in a yogurt model

Fidelis

Oliveira

Santos

et al. 2020

Journal of Dairy Science

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This work aimed to characterize the phenolic composition and in vitro antioxidant and antiproliferative properties of lyophilized camu-camu (Myrciaria dubia) seed extract (LCE), and to assess the effects of LCE on the antioxidant and sensory traits of yogurt. The LCE contained 46.3% (wt/wt) total phenolic content; the main compounds quantified were vescalagin, castalagin, gallic acid, procyanidin A2, and (−)-epicatechin. The LCE had antioxidant activity, as measured by different chemical assays (2,2-diphenyl-1-picrylhydrazyl, Folin-Ciocalteu reducing capacity, total reducing capacity, ferric reducing antioxidant power, and Cu 2+ chelating capacity), and inhibited the cell proliferation of HepG2 cells (human hepatoma carcinoma; IC 50 = 1,116 µg/ mL) and Caco-2 cells (human colorectal adenocarcinoma epithelial cells; IC 50 = 608.5 µg/mL). In addition, LCE inhibited the in vitro activity of α-amylase, α-glucosidase, and angiotensin-converting enzyme, and protected DNA from peroxyl radical-induced scission. When added to yogurts, different concentrations of LCE (0, 0.25, 0.5, 0.75, and 1.0 g/100 g) increased the chemical antioxidant and reducing capacities. The camu-camu yogurt containing LCE at 0.25 g/100 g had an acceptance index of 84%, showing that camu-camu seed extract may be a potential ingredient for addition to yogurts.

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Section: Introductionmentioning

confidence: 99%

From byproduct to a functional ingredient: Camu-camu (Myrciaria dubia) seed extract as an antioxidant agent in a yogurt model

Fidelis

Oliveira

Santos

et al. 2020

Journal of Dairy Science

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“…In general, the harmful effects of reactive oxygen species on cells are mainly composed of DNA damage, lipid peroxidation and protein oxidation [20]. Overproduction of ROS induced by PM 2.5 exposure has been associated with cell homeostasis imbalance, mitochondrial damage and apoptosis [21,22].…”

Section: Introductionmentioning

confidence: 99%

“…Activation of apoptosis pathways, consisting of receptor-mediated (extrinsic) and mitochondrial (intrinsic) pathways, is a key step in apoptosis [23,24]. The death receptor pathway is characterized by TNF-α-induced apoptosis and recruitment of caspase family proteins including caspase-8 and caspase-3 [20]. The mitochondrial pathway is triggered by the release of cytochrome-C from mitochondria, resulting in activation of caspase family proteins including caspase-3 [25].…”

Section: Introductionmentioning

confidence: 99%

The activation of antioxidant and apoptosis pathways involved in damage of human proximal tubule epithelial cells by PM2.5 exposure

et al. 2020

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Background: Exposure to airborne fine particulate matter (PM 2.5 ) has been reported to be harmful to the human kidney. However, whether the activation of oxidative stress and cell apoptosis plays key roles in the nephrotoxicity caused by PM 2.5 exposure is still poorly understood. The aim of this study was to explore the mechanism of cytotoxicity after PM 2.5 exposure in human proximal tubule epithelial cells (HK-2 cells).Results: PM 2.5 exposure resulted in a significant decrease in cell viability, with an increase in LDH release and the early kidney damage marker kidney injury molecule-1 (KIM-1) expression in a dose-dependent manner and timedependent manner. PM 2.5 exposure induced reactive oxygen species (ROS) generation and markedly elevated apoptosis in HK-2 cells. In addition, PM 2.5 exposure resulted in the activation of antioxidant pathway, as evidenced by the increased expressions of Nrf2, HO-1 and NQO1 and decreased expression of Keap1. Moreover, PM 2.5 exposure also induced the activation of apoptotic pathway, as evidenced by the increased expressions of pro-apoptotic proteins Bax, caspase-3 and caspase-8 and decreased expression of antiapoptotic protein Bcl-2. Conclusions:Our results demonstrated that both antioxidant pathway and apoptotic pathway played critical roles in the damage mediated by PM 2.5 in HK-2 cells. This study would give us a strategy to prevent the impairment of renal function by PM 2.5 induced through repression of oxidative stress and apoptosis.

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“…The observed patterns of regional contraction and expansion related to the interaction of ELS and PM2.5 may reflect cumulative allostatic load related to either psychosocial or environmental stressors. Systemic inflammation related to PM2.5 and/or to particles that directly reach the brain has been posited to promote neuroinflammation and cell death via such processes as oxidative stress, altered brain metabolism, and microglial dysfunction (35)(36)(37).…”

Section: Discussionmentioning

confidence: 99%

Severity of Early Life Stress Moderates the Effect of Fine Particle Air Pollution on Adolescent Brain Development

Miller

Dennis

et al. 2019

Preprint

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Air pollution is currently the greatest environmental threat to public health, but we know little about its effects on adolescent brain development. In this context, exposure to air pollution co-occurs, and could interact, with social factors that also affect brain development, such as early life stress (ELS). Here, we show that severity of ELS moderates the association between fine particle air pollution (particulate matter 2.5; PM2.5) and structural brain development. We interviewed adolescents about ELS, used census-tract data to characterize PM2.5 concentrations, and conducted longitudinal tensor-based morphometry to assess regional changes in brain volume over a two-year period. Across various cortical, thalamic, and white matter tract regions, there was a remarkably consistent effect of PM2.5 on volumetric change for adolescents who had experienced less, rather than more, severe ELS. Furthermore, exposure to higher levels of PM2.5 and experiencing moderate to severe ELS were associated with comparable volumetric changes in the brain in adolescence.

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Cell death pathways of particulate matter toxicity

Cited by 132 publications

References 203 publications

From byproduct to a functional ingredient: Camu-camu (Myrciaria dubia) seed extract as an antioxidant agent in a yogurt model

From byproduct to a functional ingredient: Camu-camu (Myrciaria dubia) seed extract as an antioxidant agent in a yogurt model

The activation of antioxidant and apoptosis pathways involved in damage of human proximal tubule epithelial cells by PM2.5 exposure

Severity of Early Life Stress Moderates the Effect of Fine Particle Air Pollution on Adolescent Brain Development

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