scholarly journals Drinking Ice-Cold Water Reduces the Severity of Anticancer Drug-Induced Taste Dysfunction in Mice

2020 ◽  
Vol 21 (23) ◽  
pp. 8958
Author(s):  
Ayana Osaki ◽  
Keisuke Sanematsu ◽  
Junichi Yamazoe ◽  
Fumie Hirose ◽  
Yu Watanabe ◽  
...  
Keyword(s):  
Anticancer Drug ◽  
Molecular Mechanisms ◽  
Cold Water ◽  
Taste Cell ◽  
Taste Perception ◽  
Drug Induced ◽  
Oral Cryotherapy ◽  
Taste Disorders ◽  
Taste Dysfunction ◽  
Number Of Cells

Taste disorders are common adverse effects of cancer chemotherapy that can reduce quality of life and impair nutritional status. However, the molecular mechanisms underlying chemotherapy-induced taste disorders remain largely unknown. Furthermore, there are no effective preventive measures for chemotherapy-induced taste disorders. We investigated the effects of a combination of three anticancer drugs (TPF: docetaxel, cisplatin and 5-fluorouracil) on the structure and function of mouse taste tissues and examined whether the drinking of ice-cold water after TPF administration would attenuate these effects. TPF administration significantly increased the number of cells expressing apoptotic and proliferative markers. Furthermore, TPF administration significantly reduced the number of cells expressing taste cell markers and the magnitudes of the responses of taste nerves to tastants. The above results suggest that anticancer drug-induced taste dysfunction may be due to a reduction in the number of taste cells expressing taste-related molecules. The suppressive effects of TPF on taste cell marker expression and taste perception were reduced by the drinking of ice-cold water. We speculate that oral cryotherapy with an ice cube might be useful for prophylaxis against anticancer drug-induced taste disorders in humans.

scholarly journals miR-140-5p attenuates chemotherapeutic drug-induced cell death by regulating autophagy through inositol 1,4,5-trisphosphate kinase 2 (IP3k2) in human osteosarcoma cells

2016 ◽  
Vol 36 (5) ◽  
Author(s):  
Renxiong Wei ◽  
Gang Cao ◽  
Zhouming Deng ◽  
Jiajia Su ◽  
Lin Cai
Keyword(s):  
Drug Resistance ◽  
Anticancer Drug ◽  
Molecular Mechanisms ◽  
Critical Role ◽  
Chemotherapy Resistance ◽  
Mirna Regulation ◽  
Osteosarcoma Cells ◽  
Drug Induced ◽  
Human Osteosarcoma Cells ◽  
Inositol 1,4,5 Trisphosphate

Acquisition of drug-resistant phenotypes is often associated with chemotherapy in osteosarcoma. A number of studies have demonstrated a critical role for autophagy in osteosarcoma development, therapy and drug resistance. However, the molecular mechanisms underlying the autophagy-mediated chemotherapy resistance of osteosarcoma cells remain largely unknown. In the present study, we determined the autophagy and microRNA-140 (miR-140-5p, miRBase ID: MIMAT0000431) expression induced by chemotherapeutic drugs in osteosarcoma cells. Then we determined the promotory role of miR-140-5p to the chemotherapy-induced autophagy. Our results demonstrated that miR-140-5p expression was highly induced during chemotherapy of osteosarcoma cells, and this was accompanied by up-regulated autophagy. The increased miR-140-5p expression levels up-regulated anticancer drug-induced autophagy in osteosarcoma cells and ameliorated the anticancer drug-induced cell proliferation and viability decrease. Importantly, miR-140-5p regulates this context-specific autophagy through its target, inositol 1,4,5-trisphosphate kinase 2 (IP3k2). Therefore, the results of the present study demonstrated that miR-140-5p mediated drug-resistance in osteosarcoma cells by inducing autophagy. The present study provides evidence of miRNA regulation of autophagy through modulation of IP3 signalling. The present study recognized a novel mechanism of chemoresistance in osteosarcoma cancers.

Current status of the molecular mechanisms of anticancer drug-induced apoptosis

2002 ◽  
Vol 50 (5) ◽  
pp. 343-352 ◽  
Author(s):  
Ryungsa Kim ◽  
Kazuaki Tanabe ◽  
Yoko Uchida ◽  
Manabu Emi ◽  
Hideki Inoue ◽  
...  
Keyword(s):  
Anticancer Drug ◽  
Molecular Mechanisms ◽  
Current Status ◽  
Drug Induced ◽  
Induced Apoptosis

scholarly journals POS0291 THE IMPACT OF DRUG INDUCED AND OTHER RHEUMATIC MUSCULOSKELETAL DISORDERS (MD) ON THE QUALITY OF LIFE (QOL) OF CANCER PATIENTS RECEIVED ANTICANCER DRUG TREATMENT

2021 ◽  
Vol 80 (Suppl 1) ◽  
pp. 371.1-371
Author(s):  
A. Koltakova ◽  
A. Lila ◽  
L. P. Ananyeva ◽  
A. Fedenko
Keyword(s):  
Drug Treatment ◽  
Cancer Patients ◽  
Anticancer Drug ◽  
Physical Functioning ◽  
Role Functioning ◽  
Drug Induced ◽  
Significant Difference ◽  
Eortc Qlq C30 ◽  
Eortc Qlq ◽  
The Impact

Background:Pts with cancer may have MD that can be caused by neoplastic/paraneoplastic disease, rheumatic diseases or be induced by anticancer drug treatment. There is no data about MD influence on the QoL of cancer patients. The EORTC QoL questionnaire (QLQ)-C30 is a valid questionnaire designed to assess different aspects (Global health (GH), Functional (FS) and symptoms (SS) scales) that define the QoL of cancer patients [1].Objectives:The objective of the study was to assess the impact of drug induced and other types of MD on the QoL of cancer patients that received anticancer drug treatment by using of EORTC QLQ-C30 v3.0.Methods:The sampling of 123 pts (M/F – 40/83; mean age 54.4±12.8) with breast (32,5%), gastrointestinal (17%), ovary (8%), lung (7%) and other cancer was observed by rheumatologist in the oncology outpatient clinic. All pts received anticancer drug treatment: chemotherapy (104 pts), target therapy (16 pts) checkpoint-inhibitors (14 pts), hormone therapy (13 pts) in different combinations. 102(82.9%) of 123pts had MD include arthritis (12 pts), synovitis (5 pts), arthralgia (66 pts), periarthritis (34 pts), osteodynia (13 pts). There were 58 pts (group 1; M/F – 14/44; mean age 52.5±12.2) with anticancer drug treatment induced MD and 44 pts (group 2; M/F – 16/27; mean age 57.6±13.5) with other type of MD include 26 pts with skeletal metastasis. The were 21 pts (group 3; M/F – 10/11; mean age 52.9±11.1) without MD. All pts fulfilled EORTC QLQ-C30 v3.0 (tab.1).Table 1.The median [Q1;Q3] of results of GH, SS and SS of EORTC QLQ-C30ScaleSubscaleGroup1Group2Group3GH58.3[50;58]58.3[41.7;83.3]50[50;66.7]FS*Physical functioning73.3[60;86.7]73.3[66.7;86.7]86.7[80;93]Role functioning66.7[66.7;100]83.3[50;100]100[83;100]Emotional functioning83.3[66.7;100]75[66.7;91.7]91.6[83.3;100]Social functioning83.3[66.7;100]83.3[50;100]100[83.3;100]SS*Pain33.3[0;50]16.7[0;33.3]0[0;16.7]*There are only the scores that had got a statistical difference between the groups.Kruskal-Wallis H and post-hoc (Dwass-Steel-Critchlow-Fligner (DSCF) pairwise comparisons) tests for data analysis were performed.Results:A Kruskal-Wallis H test has shown a statistically significant difference in physical (χ2(2)=7.54; p=0.023), role (χ2(2)=9.87; p=0.007), emotion (χ2(2)=7.69; p=0.021) functioning and pain (χ2(2)=8.44; p=0.015) scores between the different groups. A post-hoc test with DSCF pairwise comparisons of median has shown a statistically significant difference between 1 and 3 groups (W=3.904; p=0.016) for physical functioning, between 2 and 3 groups (W=3.35; p=0.004) for role functioning, between 2 and 3 groups (W=4.03; p=0.012) for emotional functioning, between 1 and 3 groups (W=-3.97; p=0.014) for pain scale.Conclusion:The study has shown that MD associated with anticancer drug treatment adversely affected the QoL of cancer patients received anticancer drug treatment by reducing a physical functioning and by increasing pain scores. Presence of other types of MD adversely affect the QoL by reducing emotional and role functioning.References:[1]Aaronson NK,et al.The European Organization for Research and Treatment of Cancer QLQ-C30: a quality-of-life instrument for use in international clinical trials in oncology. J Natl Cancer Inst.1993;85(5):365-376. doi:10.1093/jnci/85.5.365Disclosure of Interests:None declared

scholarly journals Mitochondrial Dynamics in Drug-Induced Liver Injury

Livers ◽  
2021 ◽  
Vol 1 (3) ◽  
pp. 102-115
Author(s):  
Anup Ramachandran ◽  
David S. Umbaugh ◽  
Hartmut Jaeschke
Keyword(s):  
Liver Injury ◽  
Molecular Mechanisms ◽  
Membrane Lipids ◽  
Mitochondrial Dynamics ◽  
Adaptive Responses ◽  
Drug Induced ◽  
Biologically Relevant ◽  
Drug Induced Liver Injury ◽  
Relevant Role ◽  
Atp Generation

Mitochondria have been studied for decades from the standpoint of metabolism and ATP generation. However, in recent years mitochondrial dynamics and its influence on bioenergetics and cellular homeostasis is also being appreciated. Mitochondria undergo regular cycles of fusion and fission regulated by various cues including cellular energy requirements and pathophysiological stimuli, and the network of critical proteins and membrane lipids involved in mitochondrial dynamics is being revealed. Hepatocytes are highly metabolic cells which have abundant mitochondria suggesting a biologically relevant role for mitochondrial dynamics in hepatocyte injury and recovery. Here we review information on molecular mediators of mitochondrial dynamics and their alteration in drug-induced liver injury. Based on current information, it is evident that changes in mitochondrial fusion and fission are hallmarks of liver pathophysiology ranging from acetaminophen-induced or cholestatic liver injury to chronic liver diseases. These alterations in mitochondrial dynamics influence multiple related mitochondrial responses such as mitophagy and mitochondrial biogenesis, which are important adaptive responses facilitating liver recovery in several contexts, including drug-induced liver injury. The current focus on characterization of molecular mechanisms of mitochondrial dynamics is of immense relevance to liver pathophysiology and have the potential to provide significant insight into mechanisms of liver recovery and regeneration after injury.

scholarly journals Cold-water immersion following sprint interval training does not alter endurance signaling pathways or training adaptations in human skeletal muscle

2017 ◽  
Vol 313 (4) ◽  
pp. R372-R384 ◽  
Author(s):  
James R. Broatch ◽  
Aaron Petersen ◽  
David J. Bishop
Keyword(s):  
Mitochondrial Biogenesis ◽  
Molecular Mechanisms ◽  
Cold Water ◽  
P53 Protein ◽  
Water Immersion ◽  
Interval Training ◽  
Cold Water Immersion ◽  
Peroxisome Proliferator ◽  
Sprint Interval Training ◽  
Single Session

We investigated the underlying molecular mechanisms by which postexercise cold-water immersion (CWI) may alter key markers of mitochondrial biogenesis following both a single session and 6 wk of sprint interval training (SIT). Nineteen men performed a single SIT session, followed by one of two 15-min recovery conditions: cold-water immersion (10°C) or a passive room temperature control (23°C). Sixteen of these participants also completed 6 wk of SIT, each session followed immediately by their designated recovery condition. Four muscle biopsies were obtained in total, three during the single SIT session (preexercise, postrecovery, and 3 h postrecovery) and one 48 h after the last SIT session. After a single SIT session, phosphorylated (p-)AMPK, p-p38 MAPK, p-p53, and peroxisome proliferator-activated receptor-γ coactivator-1α ( PGC-1α) mRNA were all increased ( P < 0.05). Postexercise CWI had no effect on these responses. Consistent with the lack of a response after a single session, regular postexercise CWI had no effect on PGC-1α or p53 protein content. Six weeks of SIT increased peak aerobic power, maximal oxygen consumption, maximal uncoupled respiration (complexes I and II), and 2-km time trial performance ( P < 0.05). However, regular CWI had no effect on changes in these markers, consistent with the lack of response in the markers of mitochondrial biogenesis. Although these observations suggest that CWI is not detrimental to endurance adaptations following 6 wk of SIT, they question whether postexercise CWI is an effective strategy to promote mitochondrial biogenesis and improvements in endurance performance.

Drug-induced taste disorders

2010 ◽  
Vol 21 (3) ◽  
pp. 240-243 ◽  
Author(s):  
B. Sadananda Naik ◽  
Nagaraj Shetty ◽  
E.V.S. Maben
Keyword(s):  
Drug Induced ◽  
Taste Disorders

Drug-induced QTc interval prolongation: A proposal towards an efficient and safe anticancer drug development

2008 ◽  
Vol 44 (4) ◽  
pp. 494-500 ◽  
Author(s):  
Giuseppe Curigliano ◽  
Gianluca Spitaleri ◽  
Howard J. Fingert ◽  
Filippo de Braud ◽  
Cristiana Sessa ◽  
...  
Keyword(s):  
Drug Development ◽  
Anticancer Drug ◽  
Qtc Interval ◽  
Interval Prolongation ◽  
Drug Induced ◽  
Qtc Interval Prolongation ◽  
Anticancer Drug Development

scholarly journals Circadian Rhythms, the Mesolimbic Dopaminergic Circuit, and Drug Addiction

2007 ◽  
Vol 7 ◽  
pp. 194-202 ◽  
Author(s):  
Colleen A. McClung
Keyword(s):  
Circadian Rhythms ◽  
Drug Addiction ◽  
Molecular Mechanisms ◽  
Dopaminergic System ◽  
Treatment Options ◽  
Drug Induced ◽  
Circadian Genes ◽  
Dopaminergic Transmission ◽  
Central Pacemaker

Drug addiction is a devastating disease that affects millions of individuals worldwide. Through better understanding of the genetic variations that create a vulnerability for addiction and the molecular mechanisms that underlie the progression of addiction, better treatment options can be created for those that suffer from this condition. Recent studies point to a link between abnormal or disrupted circadian rhythms and the development of addiction. In addition, studies suggest a role for specific genes that make up the molecular clock in the regulation of drug sensitivity, sensitization, and reward. The influence of circadian genes and rhythms on drug-induced behaviors may be mediated through the mesolimbic dopaminergic system. This system has long been implicated in the development of addiction, and recent evidence supports a regulatory role for the brain's central pacemaker and circadian gene expression in the regulation of dopaminergic transmission. This review highlights the association between circadian genes and drug addiction, and the possible role of the mesolimbic dopaminergic system in this association.

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