scholarly journals Effects of short-term clomipramine on anxiety-like behavior, cellular metabolism, and oxidative stress in primary fibroblast cells of male and female rats

2018 ◽  
Vol 6 (9) ◽  
pp. e13615 ◽  
Author(s):  
Ana G. Jimenez ◽  
Joshua D. Winward ◽  
Dana M. Smith ◽  
Christina M. Ragan
2019 ◽  
Vol 316 ◽  
pp. 60-72 ◽  
Author(s):  
Mohammad Mehdi Ommati ◽  
Omid Farshad ◽  
Hossein Niknahad ◽  
Mohammad Reza Arabnezhad ◽  
Negar Azarpira ◽  
...  

2016 ◽  
Vol 52 (1) ◽  
pp. 59-68 ◽  
Author(s):  
Gabriela Cristina Schmitt ◽  
Marcelo Dutra Arbo ◽  
Andréia Louise Lorensi ◽  
Ana Laura Bemvenuti Jacques ◽  
Sabrina Nunes do Nascimento ◽  
...  

ABSTRACT The association of p-synephrine, ephedrine, salicin, and caffeine in dietary supplements and weight loss products is very common worldwide, even though ephedrine has been prohibited in many countries. The aim of this study was to evaluate a 28-day oral exposure toxicity profile of p-synephrine, ephedrine, salicin, and caffeine mixture (10:4:6:80 w/w respectively) in male and female Wistar rats. Body weight and signs of toxicity, morbidity, and mortality were observed daily. After 28 days, animals were euthanized and blood collected for hematological, biochemical, and oxidative stress evaluation. No clinical signs of toxicity, significant weight loss or deaths occurred, nor were there any significant alterations in hematological parameters. Biochemical and oxidative stress biomarkers showed lipid peroxidation, and hepatic and renal damage (p < 0.05; ANOVA/Bonferroni) in male rats (100 and 150 mg/kg) and a reduction (p < 0.05; ANOVA/Bonferroni) in glutathione (GSH) levels in all male groups. Female groups displayed no indications of oxidative stress or biochemical alterations. The different toxicity profile displayed by male and female rats suggests a hormonal influence on mixture effects. Results demonstrated that the tested mixture can alter oxidative status and promote renal and hepatic damages.


2016 ◽  
Vol 18 (3) ◽  
pp. 9-18
Author(s):  
Ismail M. Maulood ◽  
◽  
Ali H. Ahmed ◽  
Hawzeen K. Othman ◽  
◽  
...  

2021 ◽  
pp. 074823372110105
Author(s):  
Roberta Tassinari ◽  
Andrea Martinelli ◽  
Mauro Valeri ◽  
Francesca Maranghi

Synthetic amorphous silica (SAS) nanomaterial – consisting of aggregates and agglomerates of primary silicon dioxide (SiO2) particles in the nanorange (<100 nm) – is commonly used as excipient in pharmaceuticals, in cosmetics and as food additive (E551). The available data suggest that SAS nanoparticles (NP) after intravenous (IV) exposure persist in liver and spleen; however, insufficient data exist to verify whether SAS may also induce adverse effects. The aim of the present study was to verify the potential long-term effects of SAS NP (NM-203) on spleen and liver as target organs following short-term exposure. Adult male and female Sprague-Dawley rats were treated by IV injection in the tail vein with a single (1-day) dose (SD) and repeated (5-day) doses (RD) of 20 mg/kg bw per day of SAS dispersed in sterile saline solution as vehicle. Histopathological examinations of target organs were performed after 90 days. Tissue biodistribution and full characterization of NM-203, primary particle size 13–45 nm, was performed within the framework of the Nanogenotox project. No mortality or general toxicity occurred; histopathological analysis showed splenomegaly in the RD group accompanied by inflammatory granulomas in both sexes. Granulomas were also present in liver parenchyma in the RD (both sexes) and SD groups (male only). The histopathological results indicated that SAS NP have the potential to persist and induce sex-specific chronic inflammatory lesions in spleen and liver upon short-term treatment. Overall, the data showed that the widespread use of silica in drugs might elicit chronic reactions in spleen and liver prompting to the need of further investigations on the safety of SAS NP.


Author(s):  
Xiaomeng Qiao ◽  
Mizhu Sun ◽  
Yuanyuan Chen ◽  
Wenyang Jin ◽  
Huan Zhao ◽  
...  

Abstract Aims Ethanol ingestion affects cognition and emotion, which have been attributed to the dysfunction of specific brain structures. Studies of alcoholic patients and animal models consistently identify reduced hippocampal mass as a key ethanol-induced brain adaptation. This study evaluated how neuroadaptation in the hippocampus (Hip) produced by ethanol contributed to related behavioral deficits in male and female rats. Methods Effects of acute, short-term and long-term ethanol exposure on the anxiety-like behavior and recognition memory on adult male and female Sprague–Dawley rats were assessed using elevated plus maze test and novel object recognition test, respectively. In addition, in order to investigate the direct effect of ethanol on hippocampal neurons, primary culture of hippocampal neurons was exposed to ethanol (10, 30 and 90 mM; 1, 24 and 48 h), and viability (CCK-8) and morphology (immunocytochemistry) were analyzed at structural levels. Western blot assays were used to assess protein levels of NT3-TrkC-ERK. Results Acute and short-term ethanol exposure exerted anxiolytic effects, whereas long-term ethanol exposure induced anxiogenic responses in both sexes. Short-term ethanol exposure impaired spatial memory only in female rats, whereas long-term ethanol exposure impaired spatial and recognition memory in both sexes. These behavioral impairments and ethanol-induced loss of hippocampal neurons and decreased cell viability were accompanied by downregulated NT3-TrkC-ERK pathway. Conclusion These results indicate that NT3-TrkC-ERK signaling in the Hip may play an important role in ethanol-induced structural and behavioral impairments.


1988 ◽  
Vol 7 (5) ◽  
pp. 675-685 ◽  
Author(s):  
J.F. Borzelleca ◽  
L.W. Condie ◽  
J.L. Egle

To assess adverse effects that might be caused by an event resulting in high levels of barium in drinking water, rats were gavaged with barium chloride (BaCl2 at dosage levels of 30, 100, and 300 mg/kg in a 1-day study and at 100, 145, 209, and 300 mg/kg for 10 days, and the effects were determined. LD50 values for male and female rats were found to be 419 (352–499) and 408 (342–487) mg/kg BaCl2, respectively. In the 1-day exposure study, decreases in body weight and liver/brain weight ratios and increase in kidney weight as a percentage of body weight appeared to be related to barium ingestion at 300 mg/kg. After 10 days of exposure to barium, survival of females was substantially lower at 300 mg/kg. A reduction in ovaries/brain ratio at 300 mg/kg appeared to be barium-induced. There was a decrease in BUN at 300 mg/kg in males and at all dose levels in females. No other effects were attributed to barium. Histopathological findings were negative in both the 1-and 10-day studies. It is concluded that short-term oral exposure to BaCl2 at doses up to 209 mg/kg produces no significant adverse health effects.


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