scholarly journals The knockout effect of low doses of gamma radiation on hepatotoxicity induced by Echis Coloratus snake venom in rats

2019 ◽  
Author(s):  
Esraa M. Samy ◽  
Esmat A. Shaaban ◽  
Sanaa A. Kenawy ◽  
Walaa H. Salama ◽  
Mai A. Abd El Fattah

ABSTRACTEchis Coloratus is the most medically important viper in Egypt causing several pathological effects leading to death. Gamma radiation has been used as a venom detoxifying tool in order to extend the lifespan of the immunized animals used in antivenin production process. Thus, the aim of this study is to assess the effects of increasing doses of gamma radiation on Echis Coloratus in vivo through biochemical and histological studies. The results revealed a significant increase in the levels of AST, ALT, ALP and glucose of sera collected from the rats injected with native Echis Coloratus venom compared with the non-envenomed group. On the other hand, biochemical parameters of sera of rats administrated with either 1.5 kGy or 3 kGy irradiated venom were significantly decrease compared with the native venom envenomed group at 2h, 4h and 24h post envenomation. In addition, these results were confirmed by histological studies of rats’ livers. Correspondingly, the sublethal dose injection of native Echis Coloratus venom induced significant alterations in the histological architecture of liver after 2, 4 and 24 h of injection. Concurrently, the administration of both 1.5 kGy and 3 kGy gamma irradiated venom showed fewer histological alterations compared with the native group. In conclusion, the present findings support the idea of using gamma radiation as an effective venom detoxification tool.

Author(s):  
Matthew Flegal ◽  
Melinda S. Blimkie ◽  
Heather Wyatt ◽  
Michelle Bugden ◽  
Joel Surette ◽  
...  

1997 ◽  
Vol 17 (1) ◽  
pp. 355-363 ◽  
Author(s):  
C G Maki ◽  
P M Howley

Levels of the tumor suppressor protein p53 are normally quite low due in part to its short half-life. p53 levels increase in cells exposed to DNA-damaging agents, such as radiation, and this increase is thought to be responsible for the radiation-induced G1 cell cycle arrest or delay. The mechanisms by which radiation causes an increase in p53 are currently unknown. The purpose of this study was to compare the effects of gamma and UV radiation on the stability and ubiquitination of p53 in vivo. Ubiquitin-p53 conjugates could be detected in nonirradiated and gamma-irradiated cells but not in cells which were UV treated, despite the fact that both treatments resulted in the stabilization of the p53 protein. These results demonstrate that UV and gamma radiation have different effects on ubiquitinated p53 and suggest that the UV-induced stabilization of p53 results from a loss of p53 ubiquitination. Ubiquitinated forms of p21, an inhibitor of cyclin-dependent kinases, were detected in vivo, demonstrating that p21 is also a target for degradation by the ubiquitin-dependent proteolytic pathway. However, UV and gamma radiation had no effect on the stability or in vivo ubiquitination of p21, indicating that the radiation effects on p53 are specific.


1959 ◽  
Vol 197 (4) ◽  
pp. 725-729
Author(s):  
Durwood J. Smith ◽  
Robert C. Parker ◽  
Calvin Hanna ◽  
Henry E. Curley

A battery of in vivo and in vitro tests of cardiovascular performance were used to assess the effects of whole-body gamma radiation (cobalt-60) upon the cardiovascular system of dogs. A new method for study of the pressure-volume relations of isolated surviving arteries is described. Groups of six beagles were exposed to 30 r and 100 r 22 months before death and compared with littermate controls. No differences between irradiated and control dogs could be demonstrated. Eight mongrel dogs received 300 r 30 days before death and were compared with five mongrel controls. The only significant difference observed was in the pressure-volume curves of arteries from irradiated dogs, these vessels having a greater initial tone than control arteries. It is concluded that 30 r and 100 r of whole-body gamma radiation have no demonstrable effect upon the cardiovascular system of dogs irradiated 22 months before study, but that 300 r of gamma radiation does produce a significant abnormality of blood vessels.


1989 ◽  
Vol 61 (03) ◽  
pp. 463-467 ◽  
Author(s):  
G M Smith

SummaryIn this study, 5-hydroxytryptamine (5-HT) caused a dose- dependent fall in the circulating platelet count suggesting that 5-HT receptors are activated in rat platelets to cause platelet adhesion and aggregation. When low doses of adenosine diphosphate (ADP) were simultaneously injected with 5-HT, there was a significant potentiation of the responses to ADR Ketanserin significantly reduced the potentiated responses. When higher doses of ADP were infused with bolus injections of 5-HT there was no potentiation and ketanserin did not reduce these responses. Ketanserin did not inhibit the collagen-induced fall in circulating platelet count, but did significantly increase the rate of return to the basal platelet count compared with control. 5-HT did not cause a fall in platelet count in guinea-pigs


2020 ◽  
Vol 31 (1) ◽  
pp. 3-10
Author(s):  
V. S. Nedzvetsky ◽  
V. Ya. Gasso ◽  
A. M. Hahut ◽  
I. A. Hasso

Cadmium is a common transition metal that entails an extremely wide range of toxic effects in humans and animals. The cytotoxicity of cadmium ions and its compounds is due to various genotoxic effects, including both DNA damage and chromosomal aberrations. Some bone diseases, kidney and digestive system diseases are determined as pathologies that are closely associated with cadmium intoxication. In addition, cadmium is included in the list of carcinogens because of its ability to initiate the development of tumors of several forms of cancer under conditions of chronic or acute intoxication. Despite many studies of the effects of cadmium in animal models and cohorts of patients, in which cadmium effects has occurred, its molecular mechanisms of action are not fully understood. The genotoxic effects of cadmium and the induction of programmed cell death have attracted the attention of researchers in the last decade. In recent years, the results obtained for in vivo and in vitro experimental models have shown extremely high cytotoxicity of sublethal concentrations of cadmium and its compounds in various tissues. One of the most studied causes of cadmium cytotoxicity is the development of oxidative stress and associated oxidative damage to macromolecules of lipids, proteins and nucleic acids. Brain cells are most sensitive to oxidative damage and can be a critical target of cadmium cytotoxicity. Thus, oxidative damage caused by cadmium can initiate genotoxicity, programmed cell death and inhibit their viability in the human and animal brains. To test our hypothesis, cadmium cytotoxicity was assessed in vivo in U251 glioma cells through viability determinants and markers of oxidative stress and apoptosis. The result of the cell viability analysis showed the dose-dependent action of cadmium chloride in glioma cells, as well as the generation of oxidative stress (p <0.05). Calculated for 48 hours of exposure, the LD50 was 3.1 μg×ml-1. The rates of apoptotic death of glioma cells also progressively increased depending on the dose of cadmium ions. A high correlation between cadmium concentration and apoptotic response (p <0.01) was found for cells exposed to 3–4 μg×ml-1 cadmium chloride. Moreover, a significant correlation was found between oxidative stress (lipid peroxidation) and induction of apoptosis. The results indicate a strong relationship between the generation of oxidative damage by macromolecules and the initiation of programmed cell death in glial cells under conditions of low doses of cadmium chloride. The presented results show that cadmium ions can induce oxidative damage in brain cells and inhibit their viability through the induction of programmed death. Such effects of cadmium intoxication can be considered as a model of the impact of heavy metal pollution on vertebrates.


Author(s):  
Joachim Delasoie ◽  
Aleksandar Pavic ◽  
Noémie Voutier ◽  
Sandra Vojnovic ◽  
Aurélien Crochet ◽  
...  

Synthesized and characterized a series of rhenium(I) trycarbonyl-based complexes with increased lipophilicity. Two of these novel compounds were discovered to possess remarkable anticancer, anti-angiogenic and antimetastatic activity <i>in vivo</i> (zebrafish-human CRC xenograft model), being effective at very low doses (1-3 µM). At doses as high as 250 µM the complexes did not provoke toxicity issues encountered in clinical anticancer drugs (cardio-, hepato-, and myelotoxicity). The two compounds exceed the antiproliferative and anti-angiogenic potency of clinical drugs cisplatin and sunitinib-malate, and display a large therapeutic window.


Author(s):  
Tamilarasi G P ◽  
Sabarees G

Oxidation is an essential reaction in the human body, which determines the expression of proteins in the body. This results in the altered expression like rapid growth resulting in cancers and other disorders. Many synthetic drugs are available in the market that is effective in limiting the free radical generation and the reaction of radicals with cells. Unfortunately, all those synthetic drugs were found to cause side effects and adverse effects in the body. But given the accuracy of the predictability of the results and administration, this research focuses on testing the anti-oxidant efficiency in rat models testing the biochemical parameters. Investigations have also been done on the anti-oxidant activity of Tectona, but every research was concentrated to prove the anti-oxidant activity only. extract had been tested for anti-oxidant activity by estimating various tissue parameters and it showed better activity. As predicted, there is a significant difference in the and results which can be explained are due to the physiological conditions that exist inside the body.


2016 ◽  
Vol 5 (4) ◽  
pp. 308-317
Author(s):  
Hagos Tesfay ◽  
Erika S. Bronze-Uhle ◽  
Augusto Batagin-Neto ◽  
Anna C. Véron ◽  
Thomas Geiger ◽  
...  
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