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1.
Egyptian Journal of Medical Human Genetics [The]. 2016; 17 (2): 173-184
in English | IMEMR | ID: emr-180235

ABSTRACT

Purpose: To understand the role of hyperthermia in adaptive response, Ethyl methanesulfonate [EMS] an anticarcinogenic agent, adapted meiotic cells of Poecilocerus pictus was used


Materials and methods: Based on the pilot toxicity study, the effective higher temperatures of 40[degree sign]C and 45[degree sign]C for 15 or 30 min were chosen. P. pictus were treated with conditioning [L] or challenging [H] doses of EMS and 2 h time lag [TL] between these doses [L-2 h-H] was employed. Different treatment schedules were used to analyze the influence of hyperthermia on EMS induced adaptive response namely [i] pre treatment; [ii] inter treatment; [iii] post treatment and [iv] cross adaptation. After each treatment schedule, animals were sacrificed at 12, 24, 36 and 48 h recovery times, testes were processed for meiotic chromosome preparations and anomalies were analyzed


Results: The frequencies of anomalies induced by both conditioning and challenging doses of EMS were significantly higher [p< 0.05] compared to those of the control and hyperthermia groups. The combined treatments resulted in 44-50% reduction compared to additive effect of EMS. The pre, inter, post and cross adaptation treatments with hyperthermia significantly reduced the frequencies of chromosomal anomalies compared to the challenge and combined treatments with EMS at all recovery times [p< 0.05] tested


Conclusion: There is a protection against EMS induced anomalies by hyperthermia in in vivo P. pictus. As far as our knowledge is concerned, this is the first report to demonstrate that hyperthermia enhances the EMS induced adaptive response in in vivo meiotic cells


Subject(s)
Animals , Animals, Laboratory , Male , Adaptive Immunity/drug effects , Ethyl Methanesulfonate/pharmacology , Fever , Meiosis/drug effects , Grasshoppers , Testis
2.
Egyptian Journal of Medical Human Genetics [The]. 2016; 17 (2): 201-208
in English | IMEMR | ID: emr-180239

ABSTRACT

Background: Adaptive response has been well studied by employing physical and chemical agents in normal test systems, whereas in diseased conditions very little data are available


Aim of the study: To know the presence or absence of adaptive response in diseased condition, alkylating agents such as EMS or MMS have been employed in diabetic mouse


Material and methods: To induce diabetes, mice were injected with 180 mg/kg body weight of Stz. Diabetic mice were treated with conditioning [100 mg/kg body weight of EMS or 40 mg/kg body weight of MMS], challenging [300 mg/kg body weight of EMS or 160 mg/kg body weight of MMS] and combined doses of EMS or MMS with 8 h time lag. Parallelly controls were maintained. Mice were sacrificed at 24 or 48 or 72 h RTs. Bone marrow was extracted and slides were prepared by a routine air dry technique by Evans et al. [1964] to analyze the chromosomal aberrations


Results: The results show that both the alkylating agents induced exclusively chromatid type of aberrations in both diabetic and non diabetic mice, but it is to be underlined that MMS is a more potent inducer of aberrations than EMS. Eventhough, combined treatment of EMS or MMS induced significantly less chromosomal breaks compared to challenging treatment [p< 0.05] in diabetic mice, EMS induced 40% reduction of breaks, compared to 51.74% by MMS at 24 h RT. This is true to other tested RTs


Conclusion:[1] Methylating agents are a more effective inducer of adaptive response than ethylating agents in diabetic mouse. [2] Further, it is interesting to note that the percentage reduction of chromosomal breaks in diabetics is comparatively much less than in non diabetic mouse, inferring that there is variation in adaptive response between diseased and non diseased condition


Subject(s)
Animals , Animals, Laboratory , Methyl Methanesulfonate , Ethyl Methanesulfonate , Diabetes Mellitus, Experimental , Bone Marrow Cells/drug effects , Chromosome Aberrations , Dose-Response Relationship, Immunologic , Mice
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