Understanding toxicology: mechanisms and applications

Bhatia, Madhav

doi:10.1007/s10565-016-9363-8

Cited by 7 publications

(6 citation statements)

References 18 publications

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“…The lungs exist in a high-oxygen environment. Their large surface area and high blood supply make the lungs susceptible to injuries mediated by oxidative stress [ 1 – 3 ]. Reactive oxygen species (ROS) are generated both endogenously and exogenously.…”

Section: Introductionmentioning

confidence: 99%

The pathophysiological role of mitochondrial oxidative stress in lung diseases

2017

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Mitochondria are critically involved in reactive oxygen species (ROS)-dependent lung diseases, such as lung fibrosis, asbestos, chronic airway diseases and lung cancer. Mitochondrial DNA (mtDNA) encodes mitochondrial proteins and is more sensitive to oxidants than nuclear DNA. Damage to mtDNA causes mitochondrial dysfunction, including electron transport chain impairment and mitochondrial membrane potential loss. Furthermore, damaged mtDNA also acts as a damage-associated molecular pattern (DAMP) that drives inflammatory and immune responses. In this review, crosstalk among alveolar epithelial cells, alveolar macrophages and mitochondria is examined. ROS-related transcription factors and downstream cell signaling pathways are also discussed. We conclude that targeting oxidative stress with antioxidant agents, such as thiol molecules, polyphenols and superoxide dismutase (SOD), and promoting mitochondrial biogenesis should be considered as novel strategies for treating lung diseases that currently have no effective treatment options.

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Section: Introductionmentioning

confidence: 99%

The pathophysiological role of mitochondrial oxidative stress in lung diseases

2017

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“…7B–B3 ). Meanwhile NK-1R was one of the SP receptors expressed in MCs 17 . After TEAS, NK-1R was highly expressed around SP-IP nerve fibres and was also highly expressed in MC granules.…”

Section: Resultsmentioning

confidence: 99%

“…Neuropeptide receptors NK-1R and NK-2R were found to be largely localized on MCs, and the increased expression of NK-1R and NK-2R on MCs played a role in the MC-nerve association 23 . SP was a neurotransmitter in relation to MCs activation by NK-1R 17 and this action can be diminished by application of NK-1R antagonist 24 . NK-1R antagonists bind to NK-1R on the MC, resulting in competitive or noncompetitive inhibition of the SP/NK-1R signalling pathway.…”

Section: Discussionmentioning

confidence: 99%

Neuropeptide Initiated Mast Cell Activation by Transcutaneous Electrical Acupoint Stimulation of Acupoint LI4 in Rats

Chen

Zhang

et al. 2018

Sci Rep

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Transcutaneous electrical acupoint stimulation (TEAS) has been consistently used clinically for its ease of operation, non-invasiveness and painlessness, in contrast to the characteristics of inserted needles. However, the mechanism remains unknown. The aim of this study was to investigate the local response of TEAS at Hegu acupoint (LI4). Immunohistochemistry was used to measure the expression of tryptase-positive mast cells, neuropeptides of the calcitonin gene-related peptide (CGRP) and substance P (SP) in LI4. Mast cells were also labelled with serotonin (5-HT), neurokinin-1 receptor (NK-1R) and toluidine blue. The results showed that cutaneous CGRP and SP immune-positive (CGRP-IP or SP-IP) nerve fibres in LI4 were more highly expressed. There were high degrees of mast cell aggregation and degranulation with release of 5-HT near the CGRP-IP or SP-IP nerve fibres and blood vessels after TEAS. The degranulation of mast cells (MCs) was accompanied by expression of NK-1R after TEAS. Either mast cell membrane stabilizer (Disodium cromoglycate) or NK-1R antagonist (RP 67580) diminished the accumulation and degranulation of MCs induced by TEAS. Taken together, the findings demonstrated that TEAS induced sensory nerve fibres to express CGRP and SP, which then bound to the NK-1R on MCs, after which MCs degranulated and released 5-HT, resulting in TEAS-initiated acupuncture-like signals.

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“…Bhatia [38] stated that formalin induces potent cytotoxicity due to the increased activity of caspase-9 (an initiator of apoptosis), the induction of oxidative stress, mitochondrial dysfunction, and ultimately apoptosis itself. Hegazy et al [39] observed the destruction of the genetic content of germ cells in formalin-treated mice.…”

Section: Discussionmentioning

confidence: 99%

Effect of L-carnitine on the expression of the apoptotic genes Bcl-2 and Bax

Vardiyan

Ezati

Anvari

et al. 2020

Clin Exp Reprod Med

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Objective: The genes Bcl-2 and Bax play important roles in apoptosis. Many studies have shown that formalin has a strong deleterious effect on male fertility and can induce apoptosis. L-carnitine has been reported to potentially reverse the negative effects of formalin, leading to improved spermatogenesis. In this study, we examined the levels of expression of Bcl-2 and Bax in mice treated with formalin and L-carnitine.Methods: Thirty adult BALB/c mice were categorized into three groups. The mice in the control group (n=10) were not injected with any substance. The mice in the second group (n=10) received 10 mg/kg of formalin daily via an intraperitoneal injection, while those in the final group (n=10) were intraperitoneally injected daily with a dose of 10 mg/kg of formalin and 100 mg/kg of L-carnitine. All mice were kept in isolated cages for 31 days.Results: The expression of Bax was significantly higher in the formalin-treated mice than in the mice of the control group, while the expression of Bcl-2 was significantly lower in the formalin-treated mice than in the control mice. Additionally, relative to control mice, Bcl-2 expression increased and Bax expression decreased in the mice administered both formalin and L-carnitine.Conclusion: In this study, L-carnitine was shown to augment Bcl-2 expression and to reduce Bax expression, indicating that this compound may inhibit apoptosis. Due to its positive effects, L-carnitine can be used as a prophylactic treatment for people who routinely come into direct contact with formalin as an occupational hazard.

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Understanding toxicology: mechanisms and applications

Cited by 7 publications

References 18 publications

The pathophysiological role of mitochondrial oxidative stress in lung diseases

The pathophysiological role of mitochondrial oxidative stress in lung diseases

Neuropeptide Initiated Mast Cell Activation by Transcutaneous Electrical Acupoint Stimulation of Acupoint LI4 in Rats

Effect of L-carnitine on the expression of the apoptotic genes Bcl-2 and Bax

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