Effect of acute and repeated exposure to low doses of hydrazine on hepatic microsomal enzymes and biochemical parameters in vivo

1994 ◽  
Vol 68 (4) ◽  
pp. 240-245 ◽  
Author(s):  
Andrew M. Jenner ◽  
John A. Timbrell
2012 ◽  
Vol 74 (2) ◽  
pp. 247-253
Author(s):  
Osamu NISHIKAWA ◽  
Kazuyoshi ARISHIMA ◽  
Tetsuo KOBAYASHI ◽  
Mitsuyuki SHIRAI ◽  
Masaru MURAKAMI ◽  
...  

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.


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.


Author(s):  
C.A. Moran ◽  
J. Apajalahti ◽  
A. Yiannikouris ◽  
S. Ojanperä ◽  
H. Kettunen

SummaryA pilot study was conducted to evaluate the suitability of hepatic aflatoxin (AFB1) concentration as a biomarker to assess the in vivo efficacy of a mycotoxin binder in poultry when AFB1 dietary concentrations are low. Diets containing low doses of AFB1 without or with Mycosorb® (MTB), a mycotoxin binder, were fed to broilers from 7 to 21 days of age. The accumulation of AFB1 in liver was measured by high performance liquid chromatography with a detection limit of 5 ng/kg liver. In response to 10 and 50 µg AFB1/kg feed, hepatic AFB1 accumulation was 27 and 145 ng AFB1/kg liver, respectively. At each dietary concentration of AFB1, the inclusion of 5 g MTB/kg of feed reduced (P < 0.1 for 10 μg AFB1/kg feed and P < 0.05 for 50 μg AFB1/kg feed) hepatic AFB1 accumulation by at least 50%. These results suggest that hepatic AFB1 concentration is a suitable biomarker for evaluating mycotoxin binder efficacy in poultry fed the EU maximum dietary concentration of 10 µg of AFB1/kg feed.


2018 ◽  
Vol 368 (3) ◽  
pp. 382-390 ◽  
Author(s):  
Stijn Servaes ◽  
Firat Kara ◽  
Dorien Glorie ◽  
Sigrid Stroobants ◽  
Annemie Van Der Linden ◽  
...  

2021 ◽  
Author(s):  
Esmaeil Karami ◽  
Zahra Goodarzi ◽  
Ali Ghanbari ◽  
Ahmad Reza Bandegi ◽  
Sedighe Yosefi ◽  
...  

Abstract Purpose: Environmental and occupational exposure to cadmium chloride is known to cause nephrotoxicity linked with oxidative stress in humans and animals. This study used Atorvastatin to examine its effect on cadmium chloride-induced nephrotoxicity in rat model using biochemical and histological methodologies.Methods: Experiments were performed on 56 adult male Wistar rats (200 ±20 g), randomly assigned to eight groups. Atorvastatin was administered by oral for 15 days at 20 mg/kg/day, started 7 days before cadmium chloride intraperitoneal administration (1, 2, and 3 mg/kg) for eight days. On day 16, blood samples were collected, and kidneys were excised to evaluate the biochemical and histopathological changes.Cadmium chloride significantly increased malondialdehyde (MDA), serum creatinine (Cr), blood urea nitrogen (BUN), and decreased superoxide dismutase (SOD), glutathione (GSH), and glutathione peroxidase (GPx) levels. Results: Administration of Atorvastatin (20 mg/kg) significantly improved lipid peroxidation, glutathione and activities of antioxidant enzymes and significantly decreased BUN and Creatinine. Atorvastatin clearly improved the histological changes, demonstrating its protective role against Cadmium chloride-induced kidney injury.Conclusion: Treatment with Atorvastatin significantly improves all biochemical parameters and suggests a protecting role against cadmium chloride-induced oxidative stress and histological changes in rat kidney.


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