A. Kotvytska, K. V. Tykhonovych, T. D. Kryvoruchko, K. Neporada, S. Beregovyi
{"title":"紫杉醇诱导的神经病变引起大鼠口腔器官的改变","authors":"A. Kotvytska, K. V. Tykhonovych, T. D. Kryvoruchko, K. Neporada, S. Beregovyi","doi":"10.15421/022315","DOIUrl":null,"url":null,"abstract":"The developmental mechanisms of pathological changes in the oral cavity organs, in particular, periodontal tissues and salivary glands, were elucidated in the model of paclitaxel-induced neuropathy. Experimental studies were performed on 41 white nonlinear rats of both sexes weighing 180–220 g. Toxic neuropathy was modeled by intraperitoneal injection of paclitaxel (Actavis Ltd; series 5GN5122) 2 mg/kg for 4 days (0, 2, 4 and 6). The presence of paclitaxel-induced peripheral neuropathy was confirmed by the Randall-Selitto tensoalgometric test to determine the threshold of pain sensitivity. The total proteolytic activity, total antitryptic activity, and the content of TBA-active products were determined in the homogenate of the rat submandibular and sublingual salivary glands and periodontal soft tissues, content of oxidatively modified proteins, content of average mass molecules and catalase activity; α-amylase activity was also determined in the salivary glands of animals, and the content of free fucose and glycosaminoglycans in periodontal tissues. Paclitaxel-induced neuropathy causes the development of pathological changes in the oral cavity, in particular in periodontal tissues and salivary glands of rats, as evidenced by impaired proteinase-inhibitory potential, intensification of carbonyl oxidative stress, inhibition of protein synthetic function in salivary glands and increased depolymerization of non-collagenous proteins in periodontal soft tissues.","PeriodicalId":21094,"journal":{"name":"Regulatory Mechanisms in Biosystems","volume":" ","pages":""},"PeriodicalIF":0.5000,"publicationDate":"2023-02-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Paclitaxel-induced neuropathy induces changes in oral cavity organs of rats\",\"authors\":\"A. Kotvytska, K. V. Tykhonovych, T. D. Kryvoruchko, K. Neporada, S. Beregovyi\",\"doi\":\"10.15421/022315\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"The developmental mechanisms of pathological changes in the oral cavity organs, in particular, periodontal tissues and salivary glands, were elucidated in the model of paclitaxel-induced neuropathy. Experimental studies were performed on 41 white nonlinear rats of both sexes weighing 180–220 g. Toxic neuropathy was modeled by intraperitoneal injection of paclitaxel (Actavis Ltd; series 5GN5122) 2 mg/kg for 4 days (0, 2, 4 and 6). The presence of paclitaxel-induced peripheral neuropathy was confirmed by the Randall-Selitto tensoalgometric test to determine the threshold of pain sensitivity. The total proteolytic activity, total antitryptic activity, and the content of TBA-active products were determined in the homogenate of the rat submandibular and sublingual salivary glands and periodontal soft tissues, content of oxidatively modified proteins, content of average mass molecules and catalase activity; α-amylase activity was also determined in the salivary glands of animals, and the content of free fucose and glycosaminoglycans in periodontal tissues. Paclitaxel-induced neuropathy causes the development of pathological changes in the oral cavity, in particular in periodontal tissues and salivary glands of rats, as evidenced by impaired proteinase-inhibitory potential, intensification of carbonyl oxidative stress, inhibition of protein synthetic function in salivary glands and increased depolymerization of non-collagenous proteins in periodontal soft tissues.\",\"PeriodicalId\":21094,\"journal\":{\"name\":\"Regulatory Mechanisms in Biosystems\",\"volume\":\" \",\"pages\":\"\"},\"PeriodicalIF\":0.5000,\"publicationDate\":\"2023-02-07\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Regulatory Mechanisms in Biosystems\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.15421/022315\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q4\",\"JCRName\":\"BIOLOGY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Regulatory Mechanisms in Biosystems","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.15421/022315","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q4","JCRName":"BIOLOGY","Score":null,"Total":0}
Paclitaxel-induced neuropathy induces changes in oral cavity organs of rats
The developmental mechanisms of pathological changes in the oral cavity organs, in particular, periodontal tissues and salivary glands, were elucidated in the model of paclitaxel-induced neuropathy. Experimental studies were performed on 41 white nonlinear rats of both sexes weighing 180–220 g. Toxic neuropathy was modeled by intraperitoneal injection of paclitaxel (Actavis Ltd; series 5GN5122) 2 mg/kg for 4 days (0, 2, 4 and 6). The presence of paclitaxel-induced peripheral neuropathy was confirmed by the Randall-Selitto tensoalgometric test to determine the threshold of pain sensitivity. The total proteolytic activity, total antitryptic activity, and the content of TBA-active products were determined in the homogenate of the rat submandibular and sublingual salivary glands and periodontal soft tissues, content of oxidatively modified proteins, content of average mass molecules and catalase activity; α-amylase activity was also determined in the salivary glands of animals, and the content of free fucose and glycosaminoglycans in periodontal tissues. Paclitaxel-induced neuropathy causes the development of pathological changes in the oral cavity, in particular in periodontal tissues and salivary glands of rats, as evidenced by impaired proteinase-inhibitory potential, intensification of carbonyl oxidative stress, inhibition of protein synthetic function in salivary glands and increased depolymerization of non-collagenous proteins in periodontal soft tissues.