Exposure to ozone induces a systemic inflammatory response: possible source of the neurological alterations induced by this gas

González-Guevara, Edith; Martínez-Lazcano, Juan Carlos; Custodio, Verónica; Hernández-Cerón, Miguel; Rubio, Carmen; Paz, Carlos

doi:10.3109/08958378.2014.922648

Cited by 50 publications

(21 citation statements)

References 54 publications

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“…In our O 3 exposure paradigm, we did not observe the hallmarks of neuroinflammation, such as reactive gliosis or up-regulation of proinflammatory cytokines in the brain. This is seemingly in contrast to the findings of other groups, who have reported that reactive microgliosis or the induction of proinflammatory cytokines in the brain occurs in O 3 -exposed rats (9,87). It is possible that species differences could account for different neuroinflammatory responses, and a potentially important difference in rats vs. mice is that SAA is not a major acute-phase protein in rats (31); however, a recent study by Mumaw et al (8) reported an observation of microgliosis in O 3 -exposed mice.…”

Section: Discussioncontrasting

confidence: 99%

“…Among the most prevalent toxicants in polluted air, O 3 has been associated with respiratory and cardiovascularrelated health issues and, more recently, has been implicated in CNS dysfunction. Such dysfunctions include cognitive decline and dementia (2)(3)(4), increased stroke risk (5)(6)(7), neuroinflammation and oxidative stress (8)(9)(10)(11)(12), and accumulation of amyloid-b and a-synuclein that are pathologic proteins in Alzheimer's disease and Parkinson's disease, respectively (11)(12)(13)(14)(15); however, the mechanisms by which O 3 exposure could adversely affect CNS function remain unknown. We posit that O 3 inhalation elevates circulating proinflammatory mediators that can access the CNS by crossing the blood-brain barrier (BBB).…”

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confidence: 99%

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Serum amyloid A: an ozone‐induced circulating factor with potentially important functions in the lung‐brain axis

et al. 2017

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Accumulating evidence suggests that O 3 exposure may contribute to CNS dysfunction. Here, we posit that inflammatory and acute-phase proteins in the circulation increase after O 3 exposure and systemically convey signals of O 3 exposure to the CNS. To model acute O 3 exposure, female Balb/c mice were exposed to 3 ppm O 3 or forced air for 2 h and were studied after 6 or 24 h. Of 23 cytokines and chemokines, only KC/CXCL1 was increased in blood 6 h after O 3 exposure. The acute-phase protein serum amyloid A (A-SAA) was significantly increased by 24 h, whereas C-reactive protein was unchanged. A-SAA in blood correlated with total leukocytes, macrophages, and neutrophils in bronchoalveolar lavage from O 3 -exposed mice. A-SAA mRNA and protein were increased in the liver. We found that both isoforms of A-SAA completely crossed the intact blood-brain barrier, although the rate of SAA2.1 influx was approximately 5 times faster than that of SAA1.1. Finally, A-SAA protein, but not mRNA, was increased in the CNS 24 h post-O 3 exposure. Our findings suggest that A-SAA is functionally linked to pulmonary inflammation in our O 3 exposure model and that A-SAA could be an important systemic signal of O 3 exposure to the CNS.-Erickson,

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Section: Discussioncontrasting

confidence: 99%

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confidence: 99%

Serum amyloid A: an ozone‐induced circulating factor with potentially important functions in the lung‐brain axis

et al. 2017

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“…Exposure to O 3 induces the formation of RONS and inflammatory cytokines in the lung tissue and the olfactory tract. In the CNS, these molecules are capable of activating NF- κ B that promotes the expression of proinflammatory genes [57, 58]. Our results showed an increase in the activation of NF- κ B in the acute phase of exposure while chronic exposure to O 3 showed a decreased activation of NF- κ B in the rat hippocampus.…”

Section: Discussionmentioning

confidence: 58%

Curcumin Exerted Neuroprotection against Ozone‐Induced Oxidative Damage and Decreased NF‐κB Activation in Rat Hippocampus and Serum Levels of Inflammatory Cytokines

Nery‐Flores

Mendoza-Magaña

Ramírez-Herrera

et al. 2018

Oxidative Medicine and Cellular Longevity

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Ozone is a harmful tropospheric pollutant, causing the formation of reactive oxygen and nitrogen species that lead to oxidative damage in living beings. NF-κB can be activated in response to oxidative damage, inducing an inflammatory response. Nowadays, there are no reliable results that consolidate the use of antioxidants to protect from damage caused by ozone, particularly in highly polluted cities. Curcumin has a strong antioxidant activity and is a potent inhibitor of NF-κB activation with no side effects. The aim of this study is to evaluate the effect of curcumin in preventive and therapeutic approaches against oxidative damage, NF-κB activation, and the rise in serum levels of IL-1β and TNF-α induced by acute and chronic exposure to ozone in rat hippocampus. One hundred male Wistar rats were distributed into five groups; the intact control, curcumin-fed control, the ozone-exposed group, and the preventive and therapeutic groups. These last two groups were exposed to ozone and received food supplemented with curcumin. Lipid peroxidation was determined by spectrophotometry, and protein oxidation was evaluated by immunodetection of carbonylated proteins and densitometry analysis. Activation of NF-κB was assessed by electrophoretic mobility shift assay (EMSA), and inflammatory cytokines (IL-1β and TNF-α) were determined by ELISA. Curcumin decreased NF-κB activation and serum levels of inflammatory cytokines as well as protein and lipid oxidation, in both therapeutic and preventive approaches. Curcumin has proven to be a phytodrug against the damage caused by the environmental exposure to ozone.

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“…To determine the expression of the GAD isoforms in the RN, western blot assays were performed as previously described (Gonzalez‐Guevara et al, ). In brief, GAD 65 was localized using a mouse monoclonal antibody (Santa Cruz, Biotechnology, Cat # sc‐377145, RRID: AB_2619725) (Table ), and GAD 67 was localized using a mouse monoclonal antibody (Santa Cruz Biotechnology, Cat # sc‐28376, RRID: AB_627650).…”

Section: Methodsmentioning

confidence: 99%

Participation of the dentate‐rubral pathway in the kindling model of epilepsy

Hernández-Cerón

Martínez-Lazcano

Rubio

et al. 2016

J of Neuroscience Research

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Lesions of the cerebellar dentate nucleus (DN) reduce the after-discharge duration induced by repetitive kindling stimulation and decrease seizures to a lower rank according to Racine's scale. The DN sends cholinergic and glutamatergic fibers to the red nucleus (RN), which is composed of glutamatergic and GABAergic cells. To test the participation of these neurotransmitters in seizures, we compared the levels of glutamate and gamma-aminobutyric acid (GABA) at the RN in a control condition, a kindled stage, and a kindled stage followed by DN lesions. We found that the kindled stage was associated with significant reductions in glutamate and GABA in the RN and that the lesions of the DN in kindled rats reversed the severity of seizures and restored the GABA levels. GAD , a GABA-synthesizing enzyme, was increased in kindled rats and decreased after DN lesions. GAD commonly appears localized at nerve terminals and synapses, and it is only activated when GABA neurotransmission occurs. Thus, it is possible that the increased expression of GAD found in kindled rats could be due to an exacerbated demand for GABA due to kindled seizures. It is known that GABA maintains the inhibitory tone that counterbalances neuronal excitation. The decreased expression of GAD found after the DN lesions indicated that the GABA-synthesizing enzyme was no longer required once it eliminated the excitatory glutamate input to the RN. We thus conclude that DN lesions and their consequent biochemical changes are capable of decreasing the generalized seizures induced by kindling stimulation. © 2016 Wiley Periodicals, Inc.

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Exposure to ozone induces a systemic inflammatory response: possible source of the neurological alterations induced by this gas

Cited by 50 publications

References 54 publications

Serum amyloid A: an ozone‐induced circulating factor with potentially important functions in the lung‐brain axis

Serum amyloid A: an ozone‐induced circulating factor with potentially important functions in the lung‐brain axis

Curcumin Exerted Neuroprotection against Ozone‐Induced Oxidative Damage and Decreased NF‐κB Activation in Rat Hippocampus and Serum Levels of Inflammatory Cytokines

Participation of the dentate‐rubral pathway in the kindling model of epilepsy

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