Mechanism, Prevention, and Treatment of Radiation-Induced Salivary Gland Injury Related to Oxidative Stress

Liu, Zijing; Dong, Lihua; Zheng, Zhuangzhuang; Liu, Shiyu; Shouliang, Gong; Meng, Lingbin; Xin, Ying; Jiang, Xin

doi:10.3390/antiox10111666

Cited by 16 publications

(19 citation statements)

References 162 publications

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“…Ionizing radiation commonly results in oxidative stress injury in salivary glands [ 24 ]. To evaluate the effects of salidroside on antioxidant defense in irradiated SMG cells, we measured the levels of MDA, CAT, and GSH as well as the activity of SOD using relevant kits.…”

Section: Resultsmentioning

confidence: 99%

Salidroside Ameliorates Radiation Damage by Reducing Mitochondrial Oxidative Stress in the Submandibular Gland

et al. 2022

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Radiotherapy for patients with head and neck cancer inevitably causes radiation damage to salivary glands (SGs). Overproduction of reactive oxygen species (ROS) leads to mitochondrial damage and is critical in the pathophysiology of SG radiation damage. However, mitochondrial-targeted treatment is unavailable. Herein, both in vitro and in vivo models of radiation-damaged rat submandibular glands (SMGs) were used to investigate the potential role of salidroside in protecting irradiated SGs. Cell morphology was observed with an inverted phase-contrast microscope. Malondialdehyde (MDA), superoxide dismutase (SOD), catalase (CAT), glutathione (GSH), mitochondrial ROS, mitochondrial membrane potential (MMP), and ATP were measured using relevant kits. The mitochondrial ultrastructure was observed under transmission electron microscopy. Cell apoptosis was determined by Western blot and TUNEL assays. Saliva was measured from Wharton’s duct. We found that salidroside protected SMG cells and tissues against radiation and improved the secretion function. Moreover, salidroside enhanced the antioxidant defense by decreasing MDA, increasing SOD, CAT, and GSH, and scavenging mitochondrial ROS. Furthermore, salidroside rescued the mitochondrial ultrastructure, preserved MMP and ATP, suppressed cytosolic cytochrome c and cleaved caspase 3 expression, and inhibited cell apoptosis. Together, these findings first identify salidroside as a mitochondrial-targeted antioxidant for preventing SG radiation damage.

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Section: Resultsmentioning

confidence: 99%

Salidroside Ameliorates Radiation Damage by Reducing Mitochondrial Oxidative Stress in the Submandibular Gland

et al. 2022

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“…Despite ongoing advancements in radiation technology, radiation damage to normal tissues is unavoidable ( Liu et al, 2021 ). Overcoming the side effects of radiotherapy remains a hot research topic.…”

Section: Inhibition Of Ferroptosis Can Reduce Radiation Damagementioning

confidence: 99%

Cooperation effects of radiation and ferroptosis on tumor suppression and radiation injury

Bian²,

Zheng³

et al. 2022

Front. Cell Dev. Biol.

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Ferroptosis is a kind of oxidative stress-dependent cell death characterized by iron accumulation and lipid peroxidation. It can work in conjunction with radiation to increase reactive oxygen species (ROS) generation and disrupt the antioxidant system, suppressing tumor progression. Radiation can induce ferroptosis by creating ROS, depleting glutathione, activating genes linked to DNA damage and increasing the expression of acyl-CoA synthetase long-chain family member 4 (ACSL4) in tumor cells. Furthermore, ferroptosis can enhance radiosensitivity by causing an iron overload, destruction of the antioxidant system, and lipid peroxidation. Radiation can also cause ferroptosis in normal cells, resulting in radiation injury. The role of ferroptosis in radiation-induced lung, intestinal, skin, and hematological injuries have been studied. In this review, we summarize the potential mechanisms linking ferroptosis, oxidative stress and radiation; analyze the function of ferroptosis in tumor suppression and radiation injury; and discuss the potential of ferroptosis regulation to improve radiotherapy efficacy and reduce adverse effects.

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“…As radiotherapy is continued, acinar cell apoptosis and acinar become atrophied and ducts dilated. At the same time, a large number of oxygen free radicals can induce cells to produce inflammatory chemokines, which further damage acinus, ducts, blood vessels and nerves 16–18 . In recent years, studies have shown that microvascular endothelial cells in salivary glands are important targets of irradiation injury 16,19 .…”

Section: Introductionmentioning

confidence: 99%

“…At the same time, a large number of oxygen free radicals can induce cells to produce inflammatory chemokines, which further damage acinus, ducts, blood vessels and nerves. 16 , 17 , 18 In recent years, studies have shown that microvascular endothelial cells in salivary glands are important targets of irradiation injury. 16 , 19 It is very important to explore effective methods to restore the damaged salivary gland tissue in this condition.…”

Section: Introductionmentioning

confidence: 99%

Tetrahedral framework nucleic acids alleviate irradiation‐induced salivary gland damage

Xie

Guo

et al. 2022

Cell Proliferation

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In this study, we investigated the role of tetrahedral framework nucleic acids (tFNAs) in irradiation-induced salivary gland damage in vitro and in vivo. Irradiation-damaged submandibular gland cells (SMGCs) were treated with different concentrations of tFNAs. Cell activity was measured by CCK-8 assay. Cell death was detected by Calcein-AM/PI double staining. Cell apoptosis was assessed by flow cytometry. The expression of apoptosis proteins and inflammatory cytokines were detected by western blot. Body weight, drinking volume, saliva flow rate and lag time was measured 8 weeks after irradiation. Micromorphological changes of submandibular gland were assessed by haematoxylin-eosin and masson staining. Cell proliferation, apoptosis and microvessel density of submandibular gland were evaluated by immunohistochemical staining. tFNAs could promote cell proliferation, inhibit cell apoptosis of irradiation-damaged SMGCs and reduce irradiation induced cell death. Mechanism studies revealed that tFNAs inhibited cell apoptosis through regulating the Bcl-2/Bax/Caspase-3 signalling pathway and inhibited the release of TNF-α, IL-1β and IL-6 to reduce cell damage caused by inflammation. Animal experiments showed that tFNAs could alleviate irradiation-induced weight loss, increased water intake, decreased saliva production and prolonged salivation lag time and could ameliorate salivary gland damage. tFNAs have a positive effect on alleviating irradiation-induced salivary gland damage and might be a promising agent for the treatment of this disease. | INTRODUCTIONRadiotherapy is a vital treatment for head and neck cancer. Approximately 80% of patients suffering from head and neck cancer have received radiotherapy. However, radiotherapy can cause many Xueping Xie and Wenjuan Ma contribute equally to this work.

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Mechanism, Prevention, and Treatment of Radiation-Induced Salivary Gland Injury Related to Oxidative Stress

Cited by 16 publications

References 162 publications

Salidroside Ameliorates Radiation Damage by Reducing Mitochondrial Oxidative Stress in the Submandibular Gland

Salidroside Ameliorates Radiation Damage by Reducing Mitochondrial Oxidative Stress in the Submandibular Gland

Cooperation effects of radiation and ferroptosis on tumor suppression and radiation injury

Tetrahedral framework nucleic acids alleviate irradiation‐induced salivary gland damage

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