Cancer-Induced Oxidative Stress and Pain

Nashed, Mina G.; Balenko, Matthew D.; Singh, Gurmit

doi:10.1007/s11916-013-0384-1

Cited by 16 publications

(11 citation statements)

References 84 publications

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“…These results suggested that oxidative stress plays a critical role in acute and chronic itch. Interestingly, oxidative stress has also been demonstrated to contribute to the pathogenesis of chronic inflammatory and neuropathic pain [54][55][56][57]. So, our results also suggest that chronic itch shares mechanisms with chronic pain, especially the critical contribution of oxidative stress [2,49,58].…”

Section: Discussionsupporting

confidence: 65%

Antioxidants Attenuate Acute and Chronic Itch: Peripheral and Central Mechanisms of Oxidative Stress in Pruritus

et al. 2016

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Itch (pruritus) is one of the most disabling syndromes in patients suffering from skin, liver, or kidney diseases. Our previous study highlighted a key role of oxidative stress in acute itch. Here, we evaluated the effects of antioxidants in mouse models of acute and chronic itch and explored the potential mechanisms. The effects of systemic administration of the antioxidants N-acetyl-L-cysteine (NAC) and N-tert-butyl-α-phenylnitrone (PBN) were determined by behavioral tests in mouse models of acute itch induced by compound 48/80 or chloroquine, and chronic itch by treatment with a mixture of acetone-diethyl-ether-water. We found that systemic administration of NAC or PBN significantly alleviated compound 48/80- and chloroquine-induced acute itch in a dose-dependent manner, attenuated dry skin-induced chronic itch, and suppressed oxidative stress in the affected skin. Antioxidants significantly decreased the accumulation of intracellular reactive oxygen species directly induced by compound 48/80 and chloroquine in the cultured dorsal root ganglia-derived cell line ND7-23. Finally, the antioxidants remarkably inhibited the compound 48/80-induced phosphorylation of extracellular signal-regulated kinase in the spinal cord. These results indicated that oxidative stress plays a critical role in acute and chronic itch in the periphery and spinal cord and antioxidant treatment may be a promising strategy for anti-itch therapy.

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Section: Discussionsupporting

confidence: 65%

Antioxidants Attenuate Acute and Chronic Itch: Peripheral and Central Mechanisms of Oxidative Stress in Pruritus

et al. 2016

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“…Several studies have demonstrated the participation of varied pathways and mediators involved in cancer pain development, such as cytokines [ 8 – 10 ], spinal glial activation [ 11 – 14 ], transient receptor potential vanilloid receptor 1 (TRPV1), acid-sensing ion channels (ASICs), bradykinin, adenosine triphosphate (ATP), endothelin [ 15 ], reactive oxygen species [ 16 ], and intracellular signaling pathway such as mitogen-activated protein kinases p38 [ 17 ] and JNK [ 18 ]. Cancer pain mechanisms are also dependent on the cancer type implicating that some slight variations in the mechanisms or role of a certain pathway may be greater depending on cancer type.…”

Section: Introductionmentioning

confidence: 99%

Quercetin Reduces Ehrlich Tumor-Induced Cancer Pain in Mice

Calixto-Campos

Corrêa

Carvalho

et al. 2015

Analytical Cellular Pathology

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Cancer pain directly affects the patient's quality of life. We have previously demonstrated that the subcutaneous administration of the mammary adenocarcinoma known as Ehrlich tumor induces pain in mice. Several studies have shown that the flavonoid quercetin presents important biological effects, including anti-inflammatory, antioxidant, analgesic, and antitumor activity. Therefore, the analgesic effect and mechanisms of quercetin were evaluated in Ehrlich tumor-induced cancer pain in mice. Intraperitoneal (i.p.) treatments with quercetin reduced Ehrlich tumor-induced mechanical and thermal hyperalgesia, but not paw thickness or histological alterations, indicating an analgesic effect without affecting tumor growth. Regarding the analgesic mechanisms of quercetin, it inhibited the production of hyperalgesic cytokines IL-1β and TNFα and decreased neutrophil recruitment (myeloperoxidase activity) and oxidative stress. Naloxone (opioid receptor antagonist) inhibited quercetin analgesia without interfering with neutrophil recruitment, cytokine production, and oxidative stress. Importantly, cotreatment with morphine and quercetin at doses that were ineffective as single treatment reduced the nociceptive responses. Concluding, quercetin reduces the Ehrlich tumor-induced cancer pain by reducing the production of hyperalgesic cytokines, neutrophil recruitment, and oxidative stress as well as by activating an opioid-dependent analgesic pathway and potentiation of morphine analgesia. Thus, quercetin treatment seems a suitable therapeutic approach for cancer pain that merits further investigation.

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“…High expression levels of system x c − in tumor cells are thought to be maintained in this environment and, consequently, tumor cell glutamate release is enhanced. 92 …”

Section: Pathophysiology Underlying Cibpmentioning

confidence: 99%

“…High expression levels of system x c in tumor cells are thought to be maintained in this environment and, consequently, tumor cell glutamate release is enhanced. 92 Tumor-derived glutamate may stimulate nociceptors by activating NMDA, α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid, and metabotropic-type glutamate receptors on peripheral endings, 1 thus leading to the persistent nociceptive state found in CIBP. Furthermore, because of glutamate's role in bone homeostasis, elevated glutamate may lead to further dysregulation of bone metabolism.…”

Section: Pathophysiology Underlying Cibpmentioning

confidence: 99%

Use of Animal Models in Understanding Cancer-induced Bone Pain

Slosky

Vanderah

2015

Cancer�Growth�Metastasis

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Many common cancers have a propensity to metastasize to bone. Although malignancies often go undetected in their native tissues, bone metastases produce excruciating pain that severely compromises patient quality of life. Cancer-induced bone pain (CIBP) is poorly managed with existing medications, and its multifaceted etiology remains to be fully elucidated. Novel analgesic targets arise as more is learned about this complex and distinct pain state. Over the past two decades, multiple animal models have been developed to study CIBP’s unique pathology and identify therapeutic targets. Here, we review animal models of CIBP and the mechanistic insights gained as these models evolve. Findings from immunocompromised and immunocompetent host systems are discussed separately to highlight the effect of model choice on outcome. Gaining an understanding of the unique neuromolecular profile of cancer pain through the use of appropriate animal models will aid in the development of more effective therapeutics for CIBP.

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Cancer-Induced Oxidative Stress and Pain

Cited by 16 publications

References 84 publications

Antioxidants Attenuate Acute and Chronic Itch: Peripheral and Central Mechanisms of Oxidative Stress in Pruritus

Antioxidants Attenuate Acute and Chronic Itch: Peripheral and Central Mechanisms of Oxidative Stress in Pruritus

Quercetin Reduces Ehrlich Tumor-Induced Cancer Pain in Mice

Use of Animal Models in Understanding Cancer-induced Bone Pain

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