• Title/Summary/Keyword: lung toxicity

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Systematic Analysis of Icotinib Treatment for Patients with Non-Small Cell Lung Cancer

  • Shi, Bing;Zhang, Xiu-Bing;Xu, Jian;Huang, Xin-En
    • Asian Pacific Journal of Cancer Prevention
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    • v.16 no.13
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    • pp.5521-5524
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    • 2015
  • Purpose: This analysis was conducted to evaluate the efficacy and safety of icotinib based regimens in treating patients with non-small cell lung cancer (NSCLC). Methods: Clinical studies evaluating the efficacy and safety of icotinib-based regimens with regard to response and safety for patients with NSCLC were identified using a predefined search strategy. Pooled response rates of treatment were calculated. Results: With icotinib-based regimens, 7 clinical studies which including 5,985 Chinese patients with NSCLC were considered eligible for inclusion. The pooled analysis suggested that, in all patients, the positive reponse rate was 30.1% (1,803/5,985) with icotinib-based regimens. Mild skin itching, rashes and diarrhea were the main side effects. No grade III or IV renal or liver toxicity was observed. No treatment-related death occurred in patients treated with icotinib-based regimens. Conclusions: This evidence based analysis suggests that icotinib based regimens are associated with mild response rate and acceptable toxicity for treating Chinese patients with NSCLC.

Pulmonary Fibrosis caused by Asbestos Fibers in the Respiratory Airway

  • Jung, Ji-Woo;Kim, Eung-Sam
    • Biomedical Science Letters
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    • v.27 no.3
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    • pp.111-120
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    • 2021
  • Asbestos products had been widely used until 2007 in Korea since the 1930s. A total ban on their production and applications has been imposed because of the toxic effect of asbestos fibers on the human health. The inhaled asbestos fibers increase reactive oxygen species and inflammatory reactions in the respiratory airway including the alveolar sac, resulting in DNA damages and secretion of several inflammatory cytokines or chemokines. These paracrine communications promote the proliferation of fibroblasts and the synthesis of collagen fibers, thereby depositing them into the extracellular matrix at the interstitial space of alveoli. The fibrotic tissue hindered the gas exchange in the alveolus. This reviews describes not only the cytotoxic effects of asbestos fibers with different physical or chemical characteristics but also the interaction of cells that make up the respiratory airway to understand the molecular or cellular mechanisms of asbestos fiber-induced toxicity. In addition, we propose a pulmonary toxicity research technique based on the mini-lung that can mimic human respiratory system as an alternative to overcome the limitations of the conventional risk assessment of asbestos fibers.

In Vivo Evaluation of Curcumin-loaded Nanoparticles in a A549 Xenograft Mice Model

  • Yin, Hai-Tao;Zhang, De-Geng;Wu, Xiao-Li;Huang, Xin-En;Chen, Gang
    • Asian Pacific Journal of Cancer Prevention
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    • v.14 no.1
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    • pp.409-412
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    • 2013
  • Curcumin (Cum) has been reported to have potential chemo-preventive and chemotherapeutic activity through influencing various processes, inducing cell cycle arrest, differentiation and apoptosis in a series of cancers. However, the poor solubility of Cum limits its further applications in the treatment of cancer. We have previously reported Cum-loaded nanoparticles (Cum-NPs) prepared with amphilic methoxy poly(ethylene glycol)-polycaprolactone (mPEG-PCL) block copolymers. The current study demonstrated superior antitumor efficacy of Cum-NPs over free Cum in the treatment of lung cancer. In vivo evaluation further demonstrated superior anticancer effects of Cum-NPs by delaying tumor growth compared to free Cum in an established A549 transplanted mice model. Moreover, Cum-NPs showed little toxicity to normal tissues including bone marrow, liver and kidney at a therapeutic dose. These results suggest that Cum-NPs are effective to inhibit the growth of human lung cancer with little toxicity to normal tissues, and could provide a clinically useful therapeutic regimen. They thus merit more research to evaluate the feasibility of clinical application.

Clinical Study on Mannan Peptide Combined with TP Regimen in Treating Patients with Non-small Cell Lung Cancer

  • Yan, Huai-An;Shen, Kang;Huang, Xin-En
    • Asian Pacific Journal of Cancer Prevention
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    • v.14 no.8
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    • pp.4801-4804
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    • 2013
  • Purpose: To investigate short-term response rate, quality of life and toxicities of mannan peptide combined with TP regimen in treating patients with non-small cell lung cancer (NSCLC). Patients and Methods: Forty one patients with NSCLC were divided into an experimental group treated with TP regimen combined with mannan peptide (21 patients) and a control group treated with TP alone (20 patients). Results: Response rates were 61.9% (13/21) for the experimental and 60% (12/20) for the control group (p>0.05). Regarding toxicity, white blood cell decreased more frequently in the control group (65%, 13/20) than in the experimental group (33.3%, 7/21) (p<0.05); nausea and vomiting also occurred more frequently in the control group (55%, 11/20 vs 23.8%, 5/21) (p<0.05). In terms of quality of life, this index was improved by 57.1% (12/21) and 25% (5/20) in experimental and control groups, respectively (p<0.05). Conclusions: Response rate of TP after combined with mannan peptide is mildly increased, while this combination alleviates bone marrow suppression as well as nausea and vomiting of TP, and improves quality of life when treating patients with NSCLC. However, this conclusion should be confirmed by randomized clinical trails.

EFFECT OF PHENOBARBITAL AND / OR SKF 525-A ON THE METABOLISM AND ACUTE TOXICITY OF PARATHION IN ADULT FEMALE PATS (자성 흰쥐의 파라치온 급성독성 및 대사에 미치는 페노바르비탈 및 SKF-525-A의 영향)

  • Choi, Jae-Hwa;Yim, Hye-Kyung;Kim, Young-Chul
    • Toxicological Research
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    • v.6 no.1
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    • pp.51-59
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    • 1990
  • Effects of altering hepatic mixed-function oxidase (MFO) enzyme activities on the metabolism and acute toxicity of parathio were investigated in adult female rats. In vitro hepatic metabolism of parathion to paraoxon was increased by phenobarbital pretreatment (50 mg/kg/day, ip, for 4 consecutive days) and SKF 525-A (50 mg/kg, ip, 1 hr prior to sacrifice) decreased paraoxon formation indicating that phenobarbital induces that form(s) of cytochrome P-450 catalyzing conversion of parathion to paraoxon. Degradation of paraoxon to p-nitrophenol was increased by phenobarbital pretreatment, but not affected by SKF 525-A suggesting that MFO activities play only a minor role in the detoxification of the active metabolite of this insecticide. The phenobarbital-induced increase in paraoxon formation was partially antagonized by SKF 525-A. Significant activity for both parathion activation and paraoxon degradation was also observed in the lung preparation, however, this extrahepatic parathion and paraoxon metabolizing activity was not induced by phenobarbital or inhibited by SKF 525-A pretreatment. Phenobarbital pretreatment increased paraoxon level in livers of rats when measured 3 hr following parathion injection (2 mg/kg, ip). SKF 525-A did not alter parathion or paraoxon levels in brain, blood and liver. Phenobarbital pretreatment decreased the toxicity of parathion (4mg/kg, ip) or paraoxon (1.5 mg/kg, ip) as determined by decreases in lethality and inhibition of brain and lung acetylcholinesterases. An additional SKF 525-A treatment failed to decrease the protective effects of phenobarbital against parathion or paraoxon toxicity. These results suggest that some unknown factors other than hepatic MFO induction are involved in the protective action of phenobarbital against parathion and paraoxon toxicity.

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A Case of Amiodarone-Induced Pulmonary Toxicity (Amiodarone에 의해 유발된 폐 독성 1예)

  • Shim, Jae-Jeong;Lee, Sang-Hwa;Yoo, Jae-Myung;Suh, Hong-Suk;Oh, Dong-Joo;Joh, Jae-Youn;In, Kwang-Ho;Yoo, Se-Hwa;Kang, Kyung-Ho;Kang, Eun-Young;Chae, Yang-Suk
    • Tuberculosis and Respiratory Diseases
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    • v.41 no.1
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    • pp.51-57
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    • 1994
  • Amiodarone is a potent antiarrythmic agent used in the treatment of refractory tachyarrythmias and premature ventricular contractions. Amiodarone may be responsible for the frequent and various side effects including corneal deposits, abnormal liver function test, hyperthyriodism or hypothyroidism, bluish discoloration of the skin, neuropathies, and the others. However, pulmonary toxicity is most serious adverse reaction limiting the clinical efficacy. Rescently, we experienced a case of pulmonary toxicity induced by low dose 10-month amiodarone treatment for atrial fibrilation with rapid ventricular response. Lung biopsy reveals interstitial inflammation, fibrosis, hyperplasia of pneumocytes, and foamy macrophages. Respiratory symptoms and abnormal chest X-ray findings were nearly complete cleared after using steroid and withdrawal of amiodarone. We report a case of amiodarone-induced pulmonary toxicity with literature review.

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Nasal and Pulmonary Toxicity of Titanium Dioxide Nanoparticles in Rats

  • Kwon, Soonjin;Yang, Young-Su;Yang, Hyo-Seon;Lee, Jinsoo;Kang, Min-Sung;Lee, Byoung-Seok;Lee, Kyuhong;Song, Chang-Woo
    • Toxicological Research
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    • v.28 no.4
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    • pp.217-224
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    • 2012
  • In recent decades, titanium dioxide ($TiO_2$) nanoparticles have been used in various applications, including paints, coatings, and food. However, data are lacking on the toxicological aspects associated with their use. The aim of this study was to assess the inhalation toxicity of $TiO_2$ nanoparticles in rats by using inhalation exposure. Male Wistar rats were exposed to $TiO_2$ nanoparticles for 2 weeks (6 hr/day, 5 days/week) at a mean mass concentration of $11.39{\pm}0.31mg/m^3$. We performed time-course necropsies at 1, 7, and 15 days after exposure. Lung inflammation and injury were assessed on the basis of the total and individual cell counts in bronchoalveolar lavage fluid (BALF), and by biochemical assays, including an assay for lactate dehydrogenase (LDH). Furthermore, histopathological examination was performed to investigate the lungs and nasal cavity of rats. There were no statistically significant changes in the number of BALF cells, results of biochemical assays of BALF and serum, and results of cytokine analysis. However, we did observe histopathological changes in the nasal cavity tissue. Lesions were observed at post-exposure days 1 and 7, which resolved at post-exposure day 15. We also calculated the actual amounts of $TiO_2$ nanoparticles inhaled by the rats. The results showed that the degree of toxicity induced by $TiO_2$ nanoparticles correlated with the delivered quantities. In particular, exposure to small particles with a size of approximately 20 nm resulted in toxicity, even if the total particle number was relatively low.

Acute Oral and Genetic Toxicity Study of ASCO EAQ80, a Novel Cationic Surfactant (투명 양이온 계면활성제 ASCO EAQ80에 대한 급성 경구 독성시험 및 유전 독성시험에 관한 연구)

  • Kim, Byeong-Jo;Kim, Dong-Hyeon;Lee, Jong-Ki;Moon, Surk-Sik
    • Applied Chemistry for Engineering
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    • v.20 no.2
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    • pp.145-153
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    • 2009
  • The acute oral and genetic toxicity of ASCO EAQ80 was established in this study. ASCO EAQ80, a novel cationic surfactant produced by Aekyung Speciality Chemicals Co. LTD. is currently commercialized as a clear fabric softener. In acute oral toxicity study, the 50% lethal dose $(LD_{50})$ of ASCO EAQ80 was determined to be higher than 5000 mg/kg and this product could be classified as Category 5 or Unclassified by Globally Harmonized Classification System. Also, to establish the gene-toxicity of ASCO EAQ80, we performed bacterial reversion assay against Salmonella typhimurium TA98, TA100, TA1535, TA1537, Escherichia coli WP2uvrA, and in vitro chromosomal aberration assay against Chinese hamster lung cells in the presence and absence of S-9 metabolic activation system. From these experiments, ASCO EAQ80 revealed nonmutagenic potential in S. typhimurium TA98, TA100, TA1535, TA1537, and Escherichia coli WP2uvrA both in the absence and presence of metabolic activation system. No clastogenicity of ASCO EAQ80 was observed in chromosomal aberration assay in vitro.

The Effect of Glutathione on High Dose Cisplatin-Induced Cellular Toxicity in Non-small Cell Lung Cancer Cell Lines (비소세포폐암 세포주에서 고용량 Cisplatin 세포독성에 대한 Glutathione의 효과)

  • Lee, Seung-Il;Boo, Gwi-Beom;Jang, Dai-Yong;Chung, Ki-Young;Seo, Jeoung-Gyun;Lee, Byeong-Lai;Chung, Jong-Hoon
    • Tuberculosis and Respiratory Diseases
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    • v.52 no.5
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    • pp.463-474
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    • 2002
  • Background : This study was designed to examine how glutathione, one of the nucleophilic sulfur compounds, effects the cisplatin cellular toxicity in the non-small cell lung cancer cell lines and normal lung epithelial cell line. Materials and Methods : Three cultured cell lines, the lung adenocarcinoma cell(NCL-H23), the lung squamous carcinoma cell(SK-MES-1) and the normal lung epithelial cell(L-132) line were exposed to various concentrations of cisplatin with or without glutathione. The relative viability was estimated as a means of measuring the cisplatin cellular toxicity using the MTT method. Results : In NCI-23, the response to cisplatin was sensitive but glutathione markedly increased the relative survival of the tumor cells by removing the antitumor effect of cisplatin. In both SK-MES-1 and L-132, the responses to cisplatin were less sensitive, and the chemoprotective effect of glutathione compared to and equal cisplatin dose was significantly higher in L-132 than in SK-MES-1(p<0.05). Conclusion : The protective effectes of of glutathione on cisplatin-induced cellular toxicity is more significant in normal lung epithelial cells than in squamous carcinoma cells.