Interdisciplinary Toxicology最新文献

{"title":"Antioxidant SMe1EC2 modulates pentose phosphate pathway and glutathione-dependent enzyme activities in tissues of aged diabetic rats.","authors":"Nuray Nuriye Ulusu,&nbsp;Müslüm Gök,&nbsp;Arzu Ayşe Sayin Şakul,&nbsp;Nuray Ari,&nbsp;Milan Stefek,&nbsp;Çimen Karasu","doi":"10.1515/intox-2017-0021","DOIUrl":"https://doi.org/10.1515/intox-2017-0021","url":null,"abstract":"<p><p>The pentose phosphate pathway and glutathione-associated metabolism are the main antioxidant cellular defense systems. This study investigated the effects of the powerful antioxidant SMe1EC2 (2-ethoxycarbonyl-8-methoxy-2,3,4,4a,5,9b-hexahydro-1H-pyrido[4,3-b] indolinium dichloride) on pentose phosphate pathway (PPP) and glutathione-dependent enzyme activities in aged diabetic and aged matched control rats. Diabetes was induced by streptozotocin injection in rats aged 13-15 months. Diabetic and control rats were divided into two subgroups, one untreated and one treated with SMe1EC2 (10 mg/kg/day, orally) for 4 months. SMe1EC2 ameliorated body weight loss, but not hyperglycemia of aged diabetic rats. Diabetes resulted in decreased glucose-6-phosphate dehydrogenase (G6PD), 6-phosphogluconate dehydrogenase (6PGD) and glutathione-S-transferase (GST), yet in unchanged glutathione reductase (GR) in the liver of aged diabetic rats. In the liver of the aged control rats, SMe1EC2 did not affect G6PDH, 6PGDH and GR, but it inhibited GST. SMe1EC2 also failed to affect diabetes-induced decline in 6PGDH, it ameliorated G6PDH but produced further decline in GST in the liver of aged diabetic rats. In the kidney of aged rats, G6PDH and GST were found to be comparable among the groups, but diabetes up-regulated 6PGDH and GR; these alterations were prevented by SMe1EC2. In the heart of aged diabetic rats, while GST remained unchanged, the recorded increase in G6PD, 6PGD, GR was prevented by SMe1EC2. Furthermore, an unchanged GR and remarkable increases in G6PD, 6PGD and GST were found in the lung of the aged diabetic group. These alterations were completely prevented by SMe1EC2. The results suggest that in aged rats SMe1EC2 can ameliorate the response of the kidney, heart and lung but not that of the liver against diabetes-induced glucotoxicity by interfering with the activity of redox network enzymes.</p>","PeriodicalId":13715,"journal":{"name":"Interdisciplinary Toxicology","volume":"10 4","pages":"148-154"},"PeriodicalIF":0.0,"publicationDate":"2017-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/35/41/ITX-10-148.PMC6102677.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"36429566","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"How can the process of postnatal adaptation be changed by the presence of congenital abnormalities of lip and palate.","authors":"Ingrid Brucknerová,&nbsp;Michal Dubovický,&nbsp;Eduard Ujházy","doi":"10.1515/intox-2017-0024","DOIUrl":"https://doi.org/10.1515/intox-2017-0024","url":null,"abstract":"<p><p>Despite modern approaches in molecular biology and genetics, we are still not able to identify the actual cause in more than 50% of all congenital defects. One-half of the unidentified cases is referred to as \"multifactorial\". Detailed prenatal investigation of the fetus can discover the presence of congenital abnormality, which can worsen the process of postnatal adaptation. Retrospective analysis of newborns admitted to the Neonatal Department of Intensive Medicine (NDIM) in 2012-2016 with the aim to analyze how the process of postnatal adaptation can be changed by the presence of congenital abnormalities of lip and palate. During a five-year period, 13 newborns were admitted to NDIM (2 premature; 11 term newborns). Chromosomal abnormality was confirmed in one patient (Down syndrome) and in one patient suspicion of Patau syndrome was found. Twelve newborns had complete cheilognathopalatoschisis. Two premature newborns and two term newborns had perinatal asphyxia. In this group of patients, 33% had respiratory insufficiency without the presence of congenital heart abnormality, 66% had congenital heart abnormality with respiratory insufficiency, and 2 patients had feeding problems. Only one patient had a positive family history. The diagnosis of complete cheilognathopalatoschisis was confirmed prenatally only in 9 patients. We confirmed that clinical consequences of congenital abnormalities of lip and palate depend on the nature, localization and range of abnormalities, as well as on the genetic background and accompanying congenital abnormalities. Prenatal confirmation of the presence of congenital abnormalities has an important influence on the postnatal management of a patient.</p>","PeriodicalId":13715,"journal":{"name":"Interdisciplinary Toxicology","volume":"10 4","pages":"168-171"},"PeriodicalIF":0.0,"publicationDate":"2017-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/9d/2d/ITX-10-168.PMC6102672.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"36429572","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Monotherapy of experimental metabolic syndrome: II. Study of cardiovascular effects.","authors":"Vladimír Knezl,&nbsp;Ružena Sotníková,&nbsp;Zuzana Brnoliaková,&nbsp;Tatiana Stankovičová,&nbsp;Viktor Bauer,&nbsp;Štefan Bezek","doi":"10.1515/intox-2017-0014","DOIUrl":"10.1515/intox-2017-0014","url":null,"abstract":"<p><p>Metabolic syndrome belongs to the most important risk factors of cardiovascular diseases. The aim of this study was to investigate changes in cardiovascular system induced by high cholesterol and high fat diet (HCHF) in HTG rats and their influence by a pyridoindole antioxidant - SMe1EC2 (S). The effects of S were compared with those of atorvastatin (A). Male HTG rats were fed HCHF (1% cholesterol + 7.5% lard) for 4 weeks. S and A were administered p.o., 50 mg/kg b.w. Following experimental groups were used: Wistar rats (W), hypertriglyceridemic rats (HTG), HTG rats fed HCHF (CHOL), HTG+S (S-HTG), CHOL+S (S-CHOL), and CHOL+A (A-CHOL). Values of blood pressure (BP) and selected ECG parameters were monitored in conscious animals, functions of the isolated heart and aorta were analyzed <i>ex vivo</i>. At the end of the experiment, systolic (sBP) and diastolic (dBP) blood pressure was increased in HTG and CHOL. S and A decreased BP in all treated groups. Accordingly with BP changes, the aortic endothelial function of CHOL was damaged. Both S and A administration ameliorated the endothelium-dependent relaxation to values of W. PQ and QTc intervals were prolonged in CHOL, while the treatment with S or A improved ECG findings. Prodysrhythmogenic threshold was decreased significantly in CHOL and both treatments returned it to the control values. In conclusion, HCHF increased BP, impaired endothelial relaxation of the aorta and potentiated susceptibility of myocardium to dysrhythmias. The effect of S on the changes induced by HCHF diet was more pronounced than that of A.</p>","PeriodicalId":13715,"journal":{"name":"Interdisciplinary Toxicology","volume":"10 3","pages":"86-92"},"PeriodicalIF":0.0,"publicationDate":"2017-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1515/intox-2017-0014","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"36456585","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Deleterious effects of combination of lead and β-amyloid peptides in inducing apoptosis and altering cell cycle in human neuroblastoma cells.","authors":"Ayyalasomayajula Neelima,&nbsp;Ajumeera Rajanna,&nbsp;Reddy G Bhanuprakash,&nbsp;C S Chetty,&nbsp;Challa Suresh","doi":"10.1515/intox-2017-0015","DOIUrl":"https://doi.org/10.1515/intox-2017-0015","url":null,"abstract":"<p><p>Lead (Pb) is a toxic pollutant known to cause several abnormalities related to the brain, including cognitive dysfunction, and it is ubiquitous in nature. β-amyloid peptides (AP) are crucially involved in Alzheimer's disease (AD). It has been reported that there is a connection between lead and amyloid peptides in exerting similar kinds of altered functions in the brain and long-term exposure to lead leads ultimately to increased beta amyloid formation in the brain, lethal to human brain cells. There is still a lack of information on the mechanism by which Pb affects AP formation, exerting combined toxicity in AD patients. To fill the gap, we have systematically analyzed the toxicity individually and in combination of Pb and AP in human brain cells. We found that the combination of Pb and AP exerted a higher toxicity than individual exposures in human neuroblastoma cells. The lower inhibitory concentration values were determined by both time and concentration dependent manner on using MTT assay. The data resulted in the development of enhanced toxicity on exposure to Pb with both the combinations of AP(1-40) or (25-35) and with all combinations in human brain cells compared to individual exposures to Pb (1-40) or AP(25-35). The severe apoptotic effect and alteration in cell cycle by arresting at the S-phase evidenced the increased toxicity of combinational exposure to Pb and AP on human neuroblastoma cells. Furthermore, the quantitative determination of LDH and caspase-3 activity indicated the induction of severe toxicity. We conclude that both are synergistically associated with effects such as arresting the cell cycle and triggering apoptosis during the progression of Alzheimer's disease.</p>","PeriodicalId":13715,"journal":{"name":"Interdisciplinary Toxicology","volume":"10 3","pages":"93-98"},"PeriodicalIF":0.0,"publicationDate":"2017-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1515/intox-2017-0015","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"36456586","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Chronic exposure to quinalphos shows biochemical changes and genotoxicty in erythrocytes of silver barb, <i>Barbonymus gonionotus</i>.","authors":"Islam M Sadiqul,&nbsp;Saimon Mohiful Kabir,&nbsp;Zannatul Ferdous,&nbsp;Khan Mst Mansura,&nbsp;Rahman Md Khalilur","doi":"10.1515/intox-2017-0016","DOIUrl":"https://doi.org/10.1515/intox-2017-0016","url":null,"abstract":"<p><p>An <i>in vivo</i> study was carried out on the freshwater fish <i>Barbonymus gonionotus</i> to evaluate the genotoxic effects of the organophosphate quinalphos. The fish were exposed to sub-lethal doses of quinalphos (0%, 10%, 25%, and 50% of LC₅₀) for a period of 30 days. Analysis of biochemical characteristics (protein and lipid contents of different organs), nuclear abnormalities of erythrocytes (NAE) and morphological abnormalities of erythrocytes (MAE) were performed on peripheral erythrocytes sampled at post-treatment intervals of 0 and 30 days. The biochemical results revealed a significant dose-dependent decline in protein and lipid contents and increase in the frequencies of NAE as well as MAE. Our findings also confirmed that the morphological deformations of erythrocytes in addition to NAE on fish erythrocytes <i>in vivo</i> are effective tools in determining the potential genotoxicity of organophosphates.</p>","PeriodicalId":13715,"journal":{"name":"Interdisciplinary Toxicology","volume":"10 3","pages":"99-106"},"PeriodicalIF":0.0,"publicationDate":"2017-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/6d/de/ITX-10-99.PMC6107646.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"36456587","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Comparative effects of meso-2,3- dimercaptosuccinic acid, monensin, and salinomycin on cadmium-induced brain dysfunction in cadmium-intoxicated mice.","authors":"Juliana Ivanova, Emilia Petrova, Kalina Kamenova, Yordanka Gluhcheva","doi":"10.1515/intox-2017-0017","DOIUrl":"10.1515/intox-2017-0017","url":null,"abstract":"<p><p>Cadmium (Cd) is a risk factor for neurodegenerative diseases. The purpose of this study was to compare the effects of <i>meso</i>-2,3-dimercaptosuccinic acid (DMSA) and the polyether ionophorous antibiotics monensin and salinomycin on Cd-induced neurodegenerative alterations in mice. The results show that subacute intoxication of mice with Cd (II) acetate (20 mg/kg body weight (BW) for 14 days) caused a significant accumulation of cadmium (Cd) in the brain. Treatment of Cd-exposed mice with DMSA (20 mg/kg BW for 14 days) significantly increased the Cd concentration in the brains compared to those of the Cd-treated group. However, administration of monensin (20 mg/kg BW for 14 days) or salinomycin (20 mg/kg BW for 14 days) significantly reduced the Cd concentration in the brains of Cd-treated mice compared to the toxic control group. Histopathological analysis of brain tissues from the Cd-treated mice revealed that Cd induced neuronal necrosis, characterized by many shrunken, darkly stained pyknotic neurons with prominent perineuronal spaces. Whereas monensin and salinomycin significantly reduced the adverse effects of Cd on brain morphology of Cd-treated mice, DMSA did not. Monensin slightly increased the copper and iron endogenous levels in the brains of Cd-exposed mice compared to those of the untreated mice. Salinomycin did not affect the concentrations of biometal ions in the brain of Cd-exposed mice compared to untreated controls. The results demonstrated salinomycin to be a better potential chelating agent for treatment of Cd-induced brain injury compared to DMSA and monensin.</p>","PeriodicalId":13715,"journal":{"name":"Interdisciplinary Toxicology","volume":"10 3","pages":"107-113"},"PeriodicalIF":0.0,"publicationDate":"2017-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/90/93/ITX-10-107.PMC6107650.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"36456588","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The systemic nature of mustard lung: Comparison with COPD patients.","authors":"Alireza Shahriary,&nbsp;Mostafa Ghanei,&nbsp;Hossein Rahmani","doi":"10.1515/intox-2017-0018","DOIUrl":"https://doi.org/10.1515/intox-2017-0018","url":null,"abstract":"<p><p>Sulphur mustard (SM) is a powerful blister-causing alkylating chemical warfare agent used by Iraqi forces against Iran. One of the known complications of mustard gas inhalation is mustard lung which is discussed as a phenotype of chronic obstructive pulmonary disease (COPD). In this complication, there are clinical symptoms close to COPD with common etiologies, such as in smokers. Based on information gradually obtained by conducting the studies on mustard lung patients, systemic symptoms along with pulmonary disorders have attracted the attention of researchers. Changes in serum levels of inflammatory markers, such as C-reactive protein (CRP), tumor necrosis factor alpha (TNF-α), nuclear factor κB (NF-κB), matrix metalloproteinases (MMPs), interleukin (IL), chemokines, selectins, immunoglobulins, and signs of imbalance in oxidant-antioxidant system at serum level, present the systemic changes in these patients. In addition to these, reports of extra-pulmonary complications, such as osteoporosis and cardiovascular disease are also presented. In this study, the chance of developing the systemic nature of this lung disease have been followed on using the comparative study of changes in the mentioned markers in mustard lung and COPD patients at stable phases and the mechanisms of pathogenesis and phenomena, such as airway remodeling in these patients.</p>","PeriodicalId":13715,"journal":{"name":"Interdisciplinary Toxicology","volume":"10 3","pages":"114-127"},"PeriodicalIF":0.0,"publicationDate":"2017-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1515/intox-2017-0018","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"36456058","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Monotherapy of experimental metabolic syndrome: I. Efficacy and safety.","authors":"Štefan Bezek,&nbsp;Zuzana Brnoliaková,&nbsp;Ružena Sotníková,&nbsp;Vladimír Knezl,&nbsp;Ema Paulovičová,&nbsp;Jana Navarová,&nbsp;Viktor Bauer","doi":"10.1515/intox-2017-0013","DOIUrl":"10.1515/intox-2017-0013","url":null,"abstract":"<p><p>Elevated plasma cholesterol, especially low density lipoprotein (LDL) cholesterol, is one of the major risk factors for atherosclerosis and coronary heart disease. Hereditary hypertriglyceridemic rats (hHTG) were developed as a new inbred model for the study of relationships between blood pressure and metabolic abnormalities. The aim of this work was to determine the cholesterol-lowering and antioxidant effects of the novel pyridoindol derivative SMe1EC2, compared to the cholesterol-lowering drug atorvastatin, in rats fed either standard or high-fat and high-cholesterol diet (HFC; 1% cholesterol and 7.5% lard fat). Male hHTG rats fed HFC (HTG+HFC) were administered with SMe1EC2 or atorvastatin (both 50 mg/kg/day p.o.) for 4 weeks. Physiological status of animals was monitored by the measurement of preprandial glucose levels and blood pressure. Lipid profile was characterized by the serum levels of total cholesterol (TC), HDL-, LDL-cholesterol and triglycerides (TRG). The concentration of thiobarbituric acid reactive substances (TBARS) was evaluated in the kidney, liver and serum. Further, the assessment of pro-inflammatory cytokines TNF-α, IL-1 and IL-6 in the serum was completed. Feeding the animals with HFC diet resulted in increased serum levels of TC, LDL and TRG. SMe1EC2 ameliorated serum levels of LDL in hHTG rats, both on standard and HFC diet. These effects were comparable with those of the standard hypolipidemicum atorvastatin. SMe1EC2 lowered blood pressure, tissue TBARS concentrations and serum IL-1 levels of HTG+HFC rats. Beneficial effects together with very good toxicity profile predestinate SMe1EC2 to be promising agent for further surveys related to metabolic syndrome features.</p>","PeriodicalId":13715,"journal":{"name":"Interdisciplinary Toxicology","volume":"10 3","pages":"81-85"},"PeriodicalIF":0.0,"publicationDate":"2017-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/f3/67/ITX-10-81.PMC6107645.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"36456584","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Increased intracellular and extracellular oxidant production in phagocytes of rheumatic patients treated with biological therapy - whole blood quantification.","authors":"Viera JančInová,&nbsp;Radomír Nosáľ,&nbsp;Juraj Payer,&nbsp;Zdenko Killinger","doi":"10.1515/intox-2017-0008","DOIUrl":"https://doi.org/10.1515/intox-2017-0008","url":null,"abstract":"<p><p>Infectious complications, resulting from reduced activity of immune cells, are the most severe and common adverse effects of biological therapy. This study analyzed the effect of biological therapy on blood phagocytes, focusing on the formation of reactive oxygen species (ROS), an important factor in the defence against invading pathogens. Intra- and extracellular ROS production were recorded separately, on the basis of luminol and isoluminol chemiluminescence in patients treated with antibodies against tumor necrosis factor-α or against interleukin-6 receptor. In comparison to healthy donors or to rheumatic patients treated with classical immunosuppressive drugs, biological therapy increased ROS formation in both compartments. This indicates that the anti-microbial activity of blood phagocytes was not reduced by TNFα- or IL-6-neutralizing therapy, at least in terms of ROS. The method presented does not require blood fractionation, which could modify activity of phagocytes and cause loss of some subpopulations of these cells. The technique is simple, requires microliter volumes of blood and is thus well applicable to clinical studies.</p>","PeriodicalId":13715,"journal":{"name":"Interdisciplinary Toxicology","volume":"10 2","pages":"52-55"},"PeriodicalIF":0.0,"publicationDate":"2017-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1515/intox-2017-0008","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"36410689","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Impacts of dietary exposure to sodium or potassium salts of nitrate and nitrite on the development of <i>Drosophila melanogaster</i>.","authors":"Ashim Kumar Basak,&nbsp;Tridip Chatterjee,&nbsp;Swapan Kumar Ghosh,&nbsp;Amit Chakravarty","doi":"10.1515/intox-2017-0012","DOIUrl":"10.1515/intox-2017-0012","url":null,"abstract":"<p><p>The effects of four food additives, namely sodium nitrite (NaNO₂), sodium nitrate (NaNO₃), potassium nitrite (KNO₂), and potassium nitrate (KNO₃), on animal development were evaluated by using Drosophila melanogster, a model organism. Adult male and female flies were allowed to breed in culture medium, each containing one of 4 concentrations, <i>i.e</i>.10, 20, 30 or 40 mM of the above mentioned salts. The concentration of 40 mM, NaNO₂ and KNO₂ completely arrested the development of the flies. Of the different concentrations of the four salts tested, exposure of flies to 30 mM NaNO₂ exhibited only significant delays in the initial appearances of third instar larvae, pupae and young adults, along with huge reduction in the number of pupae and young adults compared to controls. Rearrangements like inversions, deletion looping, regional shrinking, as well as highly enlarged puffing, <i>etc</i>. were also observed in the polytene chromosomes of the third instar larvae exposed to 30 mM NaNO₂. Developmental outcomes of the flies exposed to varying concentrations of NaNO₃ and KNO₃ did not differ significantly from the controls. Owing to the extensive genetic homology between Drosophila and human and the successful uses of this fly as models in developmental and toxicological studies, we speculate that the experimental results exhibited by this organism in our study strongly advocate for abstaining from the dietary use of NaNO₂ and KNO₂ during human pregnancies to avoid possible negative developmental outcomes.</p>","PeriodicalId":13715,"journal":{"name":"Interdisciplinary Toxicology","volume":"10 2","pages":"70-78"},"PeriodicalIF":0.0,"publicationDate":"2017-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/57/6a/ITX-10-70.PMC6096860.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"36410693","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}