Cytogenetic and testicular histological alterations induced by sulphur dioxide in dried apricot leather.
TL;DR: These remarkable hazardous effects of SO2 on male albino mice could be used as a potential guide for the prediction of its human health impact, and consumers could be advised to prevent excessive consumption of the drink (Qamar Al-Deen) prepared from dried apricot leather.
Abstract: Sulphur dioxide (SO2) is used as a preservative in food to prevent its discolouration, and to inhibit the growth of bacteria. Little data is available concerning its in vivo hazardous impact.The present study is therefore designed to examine the cyto-genotoxic potential and the testicular histological alterations in adult mice, induced by SO2 present in the dried apricot leather used to prepare the oriental drink Qamar Al-Deen. Two different forms of drinks were tested; cold and boiled drinks. Animals were placed into 4 groups. The first group received distilled water as a negative control.The second and third groups received orally the drink for 28 days in the form of a cold and a boiled drink, respectively. Animals of the fourth group received cyclophosphamide, they were used as a positive control for cyto-genotoxic tests. The chromosomal aberrations, as well as sperm abnormalities, were significantly elevated in animals that received the two different drink preparations. The mitotic index significantly decreased in comparison with negative and positive controls. Furthermore, histological examination showed different degrees of alterations in the testis. Our results suggest that the presence of SO2 inside the apricot leather might be responsible for these changes. Thus, these remarkable hazardous effects of SO2 on male albino mice could be used as a potential guide for the prediction of its human health impact. Furthermore, consumers could be advised to prevent excessive consumption of the drink (Qamar Al-Deen) prepared from dried apricot leather.
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TL;DR: In this article , a follow-up opinion assesses data provided by interested business operators (IBOs) and additional evidence identified in the publicly available literature, concluding that the available toxicity database was inadequate to derive an ADI and withdrew the current temporary group acceptable daily intake (ADI).
Abstract: Abstract Sulfur dioxide–sulfites (E 220–228) were re‐evaluated in 2016, resulting in the setting of a temporary ADI of 0.7 mg SO2 equivalents/kg bw per day. Following a European Commission call for data, the present follow‐up opinion assesses data provided by interested business operators (IBOs) and additional evidence identified in the publicly available literature. No new biological or toxicological data addressing the data gaps described in the re‐evaluation were submitted by IBOs. Taking into account data identified from the literature search, the Panel concluded that there was no substantial reduction in the uncertainties previously identified in the re‐evaluation. Therefore, the Panel considered that the available toxicity database was inadequate to derive an ADI and withdrew the current temporary group acceptable daily intake (ADI). A margin of exposure (MOE) approach was considered appropriate to assess the risk for these food additives. A lower confidence limit of the benchmark dose of 38 mg SO2 equivalents/kg bw per day, which is lower than the previous reference point of 70 mg SO2 equivalents/kg bw per day, was estimated based on prolonged visual evoked potential latency. An assessment factor of 80 was applied for the assessment of the MoE. At the estimated dietary exposures, when using a refined exposure scenario (Data set D), MOEs at the maximum of 95th percentile ranges were below 80 for all population groups except for adolescents. The dietary exposures estimated using the maximum permitted levels would result in MOEs below 80 in all population groups at the maximum of the ranges of the mean, and for most of the population groups at both minimum and maximum of the ranges at the 95th percentile. The Panel concluded that this raises a safety concern for both dietary exposure scenarios. The Panel also performed a risk assessment for toxic elements present in sulfur dioxide–sulfites (E 220–228), based on data submitted by IBOs, and concluded that the maximum limits in the EU specifications for arsenic, lead and mercury should be lowered and a maximum limit for cadmium should be introduced.
1 citations
TL;DR: In this paper , a simple colorimetric array has been used to detect sulfur dioxide residues in foods using principal component analysis (PCA), hierarchical clustering analysis (HCA), and linear discriminant analysis (LDA).
Abstract: Discrimination and detection of sulfur dioxide residues in foods using a simple colorimetric array have been achieved. The difference maps before and after the reaction showed that the specific color fingerprint was related to the amount of sulfur dioxide. The results of principal component analysis (PCA), hierarchical clustering analysis (HCA) and linear discriminant analysis (LDA) demonstrated that the as-fabricated colorimetric sensor array have good performance for the discrimination of sulfur dioxide and other interferents, as well as different concentrations of sulfur dioxide. Moreover, the array has been successfully applied to determine the concentration of sulfur dioxide residues in real samples and revealed good accuracy, precision and repeatability.
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TL;DR: The results suggest that sperm abnormalities might provide a rapid inexpensive mammalian screen for agents that lead to errors in the differentiation of spermatogenic stem cells in vivo and thus indicate agents which might prove to be mutagenic, teratogenic, or carcinogenic.
Abstract: The sperm of (C57BL X C3H)F1 mice were examined 1, 4, and 10 weeks after a subacute treatment with one of 25 chemicals at two or more dose levels. The fraction of sperm that were abnormal in shape was elevated above control values of 1.2-3.4% for methyl methanesulfonate, ethyl methanesulfonate, griseofulvin, benzo[a]pyrene, METEPA [tris(2-methyl-l-aziridinyl)phosphine oxide], THIO-TEPA [tris(l-aziridinyl)phosphine sulfide], mitomycin C, myleran, vinblastine sulphate, hydroxyurea, 3-methylcholanthrene, colchicine, actinomycin D, imuran, cyclophosphamide, 5-iododeoxyuridine, dichlorvos, aminopterin, and trimethylphosphate. Dimethylnitrosamine, urethane, DDT [1,1,1-trichloro-2,2-bis(p-chlorophenyl)ethane], 1,1-dimethylhydrazine, caffeine, and calcium cyclamate did not induce elevated levels of sperm abnormalities. The results suggest that sperm abnormalities might provide a rapid inexpensive mammalian screen for agents that lead to errors in the differentiation of spermatogenic stem cells in vivo and thus indicate agents which might prove to be mutagenic, teratogenic, or carcinogenic.
836 citations
"Cytogenetic and testicular histolog..." refers methods in this paper
...Morphological abnormalities of spermatozoa at 400x magnification were observed under a microscope and expressed as percentage according to the method of Wyrobek and Bruce (15)....
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...Morphological abnormalities of spermatozoa at 400x magnification were observed under a microscope and expressed as percentage according to the method of Wyrobek and Bruce (15)....
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...Wyrobek AJ, Bruce WR. Chemical induction of sperm abnormalities in mice....
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479 citations
Additional excerpts
...(14) There was a group of animals used as a positive control injected with CP (25 mg/kg b....
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TL;DR: The mouse sperm morphology test has potential use for identifying chemicals that induce spermatogenic dysfunction and perhaps heritable mutations, and is found to be highly sensitive to germ-cell mutagens.
Abstract: The literature on the mouse sperm morphology test and on other sperm tests in nonhuman mammals was reviewed (a) to evaluate the relationship of these tests to chemically induced spermatogenic dysfunction, germ-cell mutagenicity, and carcinogenicity, and (b) to make an interspecies comparison to chemicals. A total of 71 papers were reviewed. The mouse sperm morphology test was used to assess the effects of 154 of the 182 chemical agents covered. 4 other murine sperm tests were also used: the induction of acrosomal abnormalities (4 agents), reduction in sperm counts, (6 agents), motility (5 agents), and F1 sperm morphology (7 agents)). In addition, sperm tests for the spermatogenic effects of 35 agents were done in 9 nonmurine mammalian species; these included analyses for sperm count, motility, and morphology, using a large variety of study designs. For the mouse sperm morphology test, 41 agents were judged by the reviewing committee to be positive inducers of sperm-head shape abnormalities, 103 were negative, and 10 were inconclusive. To evaluate the relationship between changes in sperm morphology and germ cell mutagenicity, the effects of 41 agents on mouse sperm shape were compared to available data from 3 different mammalian germ-cell mutational tests (specific locus, heritable translocation, and dominant lethal). The mouse sperm morphology test was found to be highly sensitive to germ-cell mutagens; 100% of the known mutagens were correctly identified as positives in the sperm morphology test. Data are insufficient at present to access the rate of false positives. Although it is biologically unclear why one might expect changes in sperm morphology to be related to carcinogenesis, we found that (a) a positive response in the mouse sperm morphology test is highly specific for carcinogenic potential (100% for the agents surveyed), and (b) overall, only 50% of carcinogens were positive in the test (i.e., sensitivity approximately equal to 50%). Since many carcinogens do not produce abnormally shaped sperm even at lethal doses, negative findings with the sperm test cannot be used to classify agents as noncarcinogens. We conclude that the mouse sperm morphology test has potential use for identifying chemicals that induce spermatogenic dysfunction and perhaps heritable mutations. Insufficient numbers of chemicals agents have been studied by the other sperm tests to permit similar comparisons. A comparison of 25 chemicals tested with sperm counts, motility, and morphology in at least 2 species (including man, mouse and 9 other mammals) demonstrated good agreement in response among species. With further study, interspecies comparisons of chemically induced sperm changes may be useful for predicting and evaluating human effects.
396 citations
Additional excerpts
...Due to different kinds of mutations can induce abnormal sperm morphology, this assay is more sensitive in evaluating germ cell mutagens than other germinal mutagenicity test (20)....
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Book•
01 Jul 1980
TL;DR: Applications of Genetic Toxicology to Environmental and Human Monitoring.- Monitoring Techniques.- Occupational Monitoring.- Environmental Monitoring.- References.
Abstract: 1 Origins of Genetic Toxicology.- The History of Genetic Toxicology.- Technology Transfer to Applied Genetics.- The Components of Genetic Toxicology.- References.- 2 Fundamentals of Genetic Toxicology.- Basic Genetics for Toxicologists.- Gene Structure.- Gene Function.- The Cell Cycle and Chromosome Mechanics in Somatic and Germ Cells.- DNA Alterations Resulting in Genotoxic Effects in Cells: Mechanisms and Categorization.- A Classification Scheme for Genotoxic Effects.- Repair of DNA Damage.- References.- 3 The Consequences of Genotoxic Effects in Humans and Other Mammals.- Gene Pool Consequences.- The Direct Effect of Mutagens on the Transmissible Gene Pool.- The Relationship of Genotoxic Effects to Other Toxicologic End Points.- Relationship of Potency between Mutagenicity Assays and in Vivo Oncogenicity.- References.- 4 Screening Chemicals for Genotoxic Properties.- and Background.- Characteristics of Adequate Screening Tests.- The Type(s) and Number(s) of End Points Detected.- The Metabolic Capability of the Test or Associated Activating System.- Reliability/Reproducibility.- Facilities.- Strategies for Test Battery Development.- General Philosophy.- Approaches to Test Battery Development.- Recommendations for Group I Tests.- Interpretation of Data from Screening Tests.- The Use of Controls in in Vitro and in Vivo Testing.- Approaches to Data Analysis and Interpretation.- References.- 5 Genetic Risk Estimation.- Definition of Risk.- Risk Estimation in Somatic and Germ Cells.- Somatic Cell Risk.- Germ Cell Risk.- Relationship of the Route of Exposure to Total Body Dose.- Relationship of the Route of Exposure to Metabolism.- Blood/Gonadal Barriers.- Molecular Dosimetry of Chemical Mutagens.- Measuring the Genotoxic Effect.- Approaches to Germ Cell Risk Using Animal Models.- Extrapolating Data from Short-Term Tests to Humans.- Extrapolation of in Vitro Data Directly to in Vivo Responses.- Threshold.- References.- 6 Applications of Genetic Toxicology to Environmental and Human Monitoring.- Monitoring Techniques.- Occupational Monitoring.- Environmental Monitoring.- References.- 7 The Genetic Toxicology Laboratory.- General Laboratory Areas.- Chemical Storage and Waste Disposal.- Laboratory Safety and Employee Monitoring.- Good Laboratory Practices Requirements.- References.- 8 Descriptions of Genetic Toxicology Assays.- General Classification of Genetic Toxicology Assays.- Description of Common Assays for Gene Mutation.- Microbial.- Mammalian Cells in Vitro.- Insects.- Mammals.- Tests for Chromosome Aberrations.- Microbial.- Mammalian Cells in Vitro.- Insect Tests for Chromosome Effects.- Mammals.- Tests for Primary DNA Damage.- Microbial Tests.- Cultured Mammalian Cell Repair Assays.- SCE Analysis.- Insects.- In Vivo Mammalian Primary DNA Damage.- In Vitro Cell Transformation.- References.- 9 Sample Study Designs.- Selected Study Designs.- Protocol I: Ames Salmonella/Microsome Plate Assay.- Materials.- Test Procedures.- Evaluation Criteria.- Surviving Populations.- Dose-Response Phenomena.- Control Tests.- Evaluation Criteria for Ames Assay.- Relation between Mutagenicity and Carcinogenicity.- References.- Protocol 2: Mitotic Recombination in S. cerevisiae Strain D3.- Dosing Procedure.- Method.- Evaluation Criteria.- References.- Protocol 3: Mitotic Gene Conversion in S. cerevisiae Strain D4.- Dosing Procedure.- Method.- General Evaluation Criteria.- Surviving Populations.- Dose-Response Phenomena.- Control Tests.- Evaluation Criteria for the Preincubation Plate Incorporation Assays Using Yeast Strain D4.- Reproducibility.- References.- Protocol 4: Mitotic Recombination in S. cerevisiae Strain D5.- Dosing Procedure.- Method.- Evaluation Criteria.- References.- Protocol 5: L5178Y TK+/?Mouse Lymphoma Forward Mutation Assay.- Materials.- Indicator Cells.- Media.- Control Articles.- Sample Forms.- Experimental Design.- Dose Selection.- Mutagenicity Testing.- Preparation of 9000g Supernatant (S9).- Assay Acceptance Criteria.- Assay Evaluation Criteria.- Reference.- Protocol 6: Chromosome Aberrations in Chinese Hamster Ovary Cells.- Materials.- Indicator Cells.- Medium.- Control Articles.- Experimental Design.- Toxicity and Dose Determination.- Cell Treatment.- Preparation of S9 Reaction Mixture.- Staining and Scoring of Slides.- Evaluation Criteria.- Reference.- Protocol 7: Sister Chromatid Exchange in Human Lymphocytes.- Materials.- Experimental Design.- Option 1.- Option 2.- Staining and Scoring of Slides.- Evaluation Criteria.- Reference.- Protocol 8: Sister Chromatid Exchange in Chinese Hamster Ovary Cells.- Materials.- Experimental Design.- Toxicity and Dose Determination.- Cell Treatment.- Preparation of S9 Reaction Mixture.- Staining and Scoring of Slides.- Evaluation Criteria.- References.- Protocol 9: Determination of Unscheduled DNA Synthesis in Human WI-38 Cells.- Materials.- Experimental Design.- Dose Selection.- Nonactivation Assay.- Activation Assay.- Extraction of DNA.- DNA Analysis.- Preparation of 9000g Supernatant (S9).- Evaluation Criteria.- Reference.- Protocol 10: Unscheduled DNA Synthesis in Rat Liver Primary Cell Cultures.- Materials.- Experimental Design.- Dose Selection.- UDS Assay Method.- Evaluation Criteria.- Reference.- Protocol 11: In Vitro Transformation of BALB/3T3 Cells.- Materials.- Experimental Design.- Dose Selection.- Transformation Assay.- Scoring of Transformed Foci.- Assay Acceptance Criteria.- Assay Evaluation Criteria.- References.- Protocol 12: Microbial Host-Mediated Assay.- Materials.- Experimental Design.- Animal Husbandry.- Dose Selection.- Route of Administration.- Test and Control Articles.- Bacteria Administration and Recovery.- Cell Plating for Survival and Mutant Determinations.- References.- Protocol 13: Bone Marrow Cytogenetic Analysis in Rats.- Materials.- Experimental Design.- Animal Husbandry.- Dose Selection.- Route of Administration.- Methodology.- Evaluation Criteria.- References.- Protocol 14: Dominant Lethal Assay in Rats.- Materials.- Experimental Design.- Animal Husbandry.- Dose Selection.- Route of Administration.- Methodology.- References.- Protocol 15: Heritable Translocation Assay in Mice.- Materials.- Experimental Design.- Animal Husbandry.- Dose Selection.- Methodology.- References.- Protocol 16: Mouse Micronucleus Assay.- Materials.- Experimental Design.- Animal Husbandry.- Dose Selection.- Dosing Schedule and Route of Administration.- Extraction of Bone Marrow.- Preparation of Slides.- Screening the Slides.- Evaluation Criteria.- References.- Protocol 17: Mouse Sperm head Abnormalities.- Materials.- Experimental Design.- Animal Husbandry.- Dose Selection.- Dosing Schedule and Route of Administration.- Preparation of Sperm Suspension.- Evaluation Criteria.- References.- Protocol 18: Somatic Mutation Assay in the Mouse (Spot Test).- Materials.- Animals.- Control Articles.- Experimental Design.- Animal Husbandry.- Dose Selection.- Route of Administration.- Treatment.- Spot Observation.- References.- Protocol 19: Test for Loss of X and Y Chromosomes in D. melanogaster.- Materials.- Experimental Design.- Solubility Testing.- Palatability and Toxicity Testing.- Fertility Testing.- Test Size.- Procedure.- Collection of Males.- Dosing.- Mating and Scoring.- Data Analysis.- Reference.- Protocol 20: Heritable Translocation Test in D. melanogaster.- Materials.- Experimental Design.- Solubility Testing.- Palatability and Toxicity Testing.- Fertility Testing.- Test Size.- Procedure.- Collection of Males.- Dosing.- Mating and Scoring.- Data Analysis.- Reference.- Protocol 21: Sex-Linked Recessive Lethal Test in D. melanogaster.- Materials.- Experimental Design.- Solubility Testing.- Palatability and Toxicity Testing.- Fertility Testing.- Test Size.- Procedure.- Collection of Males.- Dosing.- Mating and Scoring.- Data Analysis.- References.- Appendices.- Appendix A: Preparation of S9 Liver Homogenates.- Induction of Microsomal Enzymes.- Preparation of the S9 Fraction.- Preparation of the S9 Mix.- References.- References.- Appendix C: Selected References and Reviews of Genetics and Genetic Toxicology.
188 citations
TL;DR: The results indicate that inhalation exposure to SO2 damages the DNA of multiple organs in addition to the lung, and suggests that this damage could result in mutation, cancer, and other diseases related to DNA damage.
Abstract: Sulfur dioxide (SO2) is a ubiquitous air pollutant produced by the burning of fossil fuels. In this study, single-cell gel electrophoresis (the Comet assay) was used to evaluate the DNA damage produced by inhalation exposure of mice to SO2. Male and female mice were housed in exposure chambers and treated with 14.00 +/- 1.25, 28.00 +/- 1.98, 56.00 +/- 3.11, and 112.00 +/- 3.69 mg/m3 SO2 for 6 hr/day for 7 days, while control groups were exposed to filtered air. Comet assays were performed on blood lymphocytes and cells from the brain, lung, liver, spleen, kidney, intestine, and testicles of the animals. SO2 caused significant, dose-dependent increases in DNA damage, as measured by Olive tail moment, in all the cell types analyzed from both sexes of mice. The results indicate that inhalation exposure to SO2 damages the DNA of multiple organs in addition to the lung, and suggests that this damage could result in mutation, cancer, and other diseases related to DNA damage. Further work will be required to understand the ultimate toxicological significance of this damage. These data also suggest that detecting DNA damage in blood lymphocytes, using the Comet assay, may serve as a useful tool for evaluating the impact of pulmonary SO2 exposure in human biomonitoring studies.
91 citations
"Cytogenetic and testicular histolog..." refers background in this paper
...(4) revealed that exposure to SO2 damage the DNA of many organs, which could lead to mutations, cancer and other diseases....
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