Effects of fullerenol nanoparticles and amifostine on radiation-induced tissue damages: Histopathological analysis

Jacević, Vesna; Jović, Danica; Kuča, Kamil; Dragojević-Simić, Viktorija; Dobric, Silva; Trajković, Sanja; Borišev, Ivana; Šegrt, Zoran; Milovanović, Zoran; Bokonjić, Dubravko; Djordjević, A.

doi:10.1016/j.jab.2016.05.004

Cited by 39 publications

(25 citation statements)

References 43 publications

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“…The intensity of hepatic and splenic lesions consisting of oedema, amount of inflammatory cells, hemorrhages, degeneration and their distribution were counted in six separate visual fields at 400× magnification. Degenerative and vascular alterations were analyzed throughout whole visual fields by using a light microscope according to the 5-point semiquantitative scale published earlier in the literature (Jaćević et al, 2016, 2017, 2018; Nežić et al, 2018). A severity grade, shown as hepatic damage score (HDS) and splenic damage score (SDS) of tissue lesions were determined for all sections of the whole tissue, and a mean hepatic and splenic were HDS and SDS determined, respectively.…”

Section: Methodsmentioning

confidence: 99%

Simvastatin Inhibits Endotoxin-Induced Apoptosis in Liver and Spleen Through Up-Regulation of Survivin/NF-κB/p65 Expression

et al. 2019

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Endotoxemia is associated by dysregulated apoptosis of immune and non-immune cells. We investigated whether simvastatin has anti-apoptotic effects, and induces hepatocytes and lymphocytes survival signaling in endotoxin-induced liver and spleen injuries. Wistar rats were divided into the groups pretreated with simvastatin (20 or 40 mg/kg, orally) prior to a non-lethal dose of lipopolysaccharide (LPS), the LPS group, and the control. The severity of tissue inflammatory injuries was expressed as hepatic damage scores (HDS) and spleen damage scores (SDS), respectively. The apoptotic cell was detected by TUNEL (Terminal deoxynucleotidyl transferase dUTP Nick End Labeling) and immunohistochemical staining (expression of cleaved caspase-3, and anti-apoptotic Bcl-xL, survivin and NF-κB/p65). Simvastatin dose-dependently abolished HDS and SDS induced by LPS ( p < 0.01), respectively. Simvastatin 40 mg/kg significantly decreased apoptotic index and caspase-3 cleavage in hepatocytes and lymphocytes ( p < 0.01 vs. LPS group, respectively), while Bcl-XL markedly increased accordingly with simvastatin doses. In the simvastatin, groups were determined markedly increased cytoplasmic expression of survivin associated with nuclear positivity of NF-κB, in both hepatocytes and lymphocytes ( p < 0.01 vs. LPS group). Cell-protective effects of simvastatin against LPS seemed to be mediated by up-regulation of survivin, which leads to reduced caspase-3 activation and inhibition of hepatocytes and lymphocytes apoptosis.

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Section: Methodsmentioning

confidence: 99%

Simvastatin Inhibits Endotoxin-Induced Apoptosis in Liver and Spleen Through Up-Regulation of Survivin/NF-κB/p65 Expression

et al. 2019

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“…The severity of heart, diaphragm and musculus popliteus lesions consisting of oedema, cellular infiltration, haemorrhages, vacuolar degeneration, necrosis, and the distribution of lesions (e.g., focal, multifocal, locally extensive, or diffuse) were assessed and graded by two independent pathologists. From each slice, whole visual fields were analyzed by using a light microscope according to the 5-point semiquantitative scale (Table 5) according to the degree and extent of the changes described above 76–79 . A severity grade was expressed as cardiac damage score (CDS), diaphragm damage score (DDS) and musculus popliteus damage score (MPDS), respectively.…”

Section: Methodsmentioning

confidence: 99%

Toxic Injury to Muscle Tissue of Rats Following Acute Oximes Exposure

Jacević

Nepovimová

Kuča

2019

Sci Rep

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Therapeutic application of newly developed oximes is limited due to their adverse effects on different tissues. Within this article, it has been investigated which morphological changes could be observed in Wistar rats after the treatment with increasing doses of selected acetyl cholinesterase reactivators - asoxime, obidoxime, K027, K048, and K075. Subsequently, heart, diaphragm and musculus popliteus were obtained for pathohistological and semiquantitative analysis 24 hrs and 7 days after im administration of a single dose of 0.1 LD50, 0.5 LD50, and 1.0 LD50 of each oxime. Different muscle damage score was based on an estimation scale from 0 (no damage) to 5 (strong damage). In rats treated with 0.1 LD50 of each oxime, muscle fibres did not show any change. The intensive degeneration was found in all muscles after treatment with 0.5 LD50 of asoxime and obidoxime, respectively. Acute toxic muscle injury was developed within 7 days following treatment with 0.5 LD50 and 1.0 LD50 of each oxime, with the highest values in K048 and K075 group (P < 0.001 vs. control and asoxime), respectively. The early muscle alterations observed in our study seem to contribute to the pathogenesis of the oxime-induced toxic muscle injury, which probably manifests as necrosis and/or inflammation.

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“…The severity of hepatic and renal lesions consisting of edema, cellular infiltration, hemorrhages, vacuolar degeneration, necrosis, and the distribution of lesions (e.g., focal, multifocal, locally extensive, or diffuse) were assessed and graded by two independent pathologists. From each slice, whole visual fields were analyzed by using light microscope according to the 5-point semiquantitative scale previously described [32,73]. A severity grade was expressed as hepatic damage score (HDS) and renal damage score (RDS), and the exact method of calculation is shown in Table 4 and Table 5, respectively.…”

Section: Methodsmentioning

confidence: 99%

The Efficacy of Amifostine against Multiple-Dose Doxorubicin-Induced Toxicity in Rats

Jaćević

Dragojević-Simić

Tatomirovic

et al. 2018

IJMS

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Amifostine is well known cytoprotector which is efficient when administered before a wide range of antineoplastic agents. The aim of our study was to investigate amifostine effects on doxorubicin-induced toxic changes in rats. Amifostine (75 mg/kg ip) was given 30 min before each dose of doxorubicin (cumulatively 20 mg/kg ip, for 28 days). The animals’ whole-body, liver, and kidney weight, serum biochemical examination, as well as microscopic examination of bone marrow, peripheral blood, liver, and kidney, were done on day 56 of the study. Hepatic and renal alterations were carefully quantified by semiquantitative grading scales—hepatic and renal damage score, respectively. In amifostine-pretreated rats, the number of peripheral blood leukocytes was significantly higher in comparison to doxorubicin-only treated group, preferentially protecting neutrophils. In the same group of rats, hepatic and renal alterations associated with polymorphonuclear cell infiltrates were significantly less severe than those observed in animals receiving only doxorubicin. Our results showed that amifostine successfully protected rats against multiple-dose doxorubicin-induced toxicity by complex, and still not fully elucidated mechanisms of action.

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Effects of fullerenol nanoparticles and amifostine on radiation-induced tissue damages: Histopathological analysis

Cited by 39 publications

References 43 publications

Simvastatin Inhibits Endotoxin-Induced Apoptosis in Liver and Spleen Through Up-Regulation of Survivin/NF-κB/p65 Expression

Simvastatin Inhibits Endotoxin-Induced Apoptosis in Liver and Spleen Through Up-Regulation of Survivin/NF-κB/p65 Expression

Toxic Injury to Muscle Tissue of Rats Following Acute Oximes Exposure

The Efficacy of Amifostine against Multiple-Dose Doxorubicin-Induced Toxicity in Rats

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