Impact of zinc oxide nanoparticles on thioredoxin‐interacting protein and asymmetric dimethylarginine as biochemical indicators of cardiovascular disorders in gamma‐irradiated rats

Abstract

Nanoparticle is a microscopic particle that has been existed in a wide range of biotechnological purposes. Zinc oxide nanoparticles (ZnO‐NPs) have fewer environmental hazards and have shown positive impacts in the medical field. This work aimed to observe the effects of low and high doses of ZnO‐NPs on heart injury induced by ionizing radiation (IR). Animals were irradiated by 8 Gy of gamma rays and ZnO‐NPs (10 and 300 mg/Kg/day) were orally delivered to rats 1 hour after irradiation. Animals were dissected on 15th day postirradiation. Data showed that the oxidative damage resulted from radiation exposure, appeared by marked increments in the malondialdehyde (MDA) content and the level and protein expression of thioredoxin‐interacting protein (TXNIP) with a noticeable decline in the level and expression of thioredoxin 1 (Trx‐1) and thioredoxin reductase (TrxR), as well as glutathione (GSH) level and the activity of superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx). Moreover, radiation‐induced inflammation, manifested by a noticeable elevation in the level of tumor necrotic factor‐alpha (TNF‐α), interleukin‐18 (IL‐18), and C‐reactive protein (CRP). Additionally, endothelial dysfunction marked with a high level of asymmetric dimethylarginine (ADMA), total nitrite/nitrate (NOx), intercellular adhesion molecule 1 (ICAM‐1), homocysteine (Hcy), creatine kinase (CK‐MB), cardiac troponin‐I (cTn‐I), and lactate dehydrogenase (LDH). In addition, a decrease of zinc (Zn) level in the cardiac tissue was recorded. ZnO‐NPs treatment (10 mg/kg) mitigated the oxidative stress and inflammation effects on the cardiovascular tissue through the positive modulations in the studied parameters. In contrast, ZnO‐NPs treatment (300 mg/kg) induced cardiovascular toxicity of normal rats and elevated the deleterious effects of radiation. In conclusion, ZnO‐NPs at a low dose could mitigate the adverse effects on cardiovascular tissue induced by radiation during its applications, while the high dose showed morbidity and mortality in normal and irradiated rats.

Identification of Potential Radiation Responsive Metabolic Biomarkers in Plasma of Rats Exposed to Different Doses of Cobalt-60 Gamma Rays

“…32 Symmetric dimethylarginine has changed in rats with cardiovascular disorders after gamma rays irradiation. 33 L-palmitoylcarnitine is not found to have a direct relationship with IR, but as a type of fatty acylation, palmitoylation plays an essential role in many biological processes, such as apoptosis and proliferation. 34 N-acetylornithine is identified as minor components of deproteinized plasma of humans, and 2-aminooctanoic acid is a fatty acid that modifies a lactoferricin B peptide to improve antimicrobial activity.…”

Pathological Roles of Mitochondrial Oxidative Stress and Mitochondrial Dynamics in Cardiac Microvascular Ischemia/Reperfusion Injury

“…Of note, the increase in mtROS in endothelial cells under I/R injury may also result from excessive inflammation response because myeloperoxidase (MPO) expression, a neutrophil infiltration marker, is upregulated in reperfused heart [101,102]. Increased thioredoxin-interacting protein (TXNIP) and a noticeable decline in the levels of thioredoxin 1 (Trx-1), thioredoxin reductase (TrxR), glutathione (GSH), catalase (CAT), and glutathione peroxidase (GPx) may also contribute to endothelial oxidative stress [103]. In order to attenuate oxidative stress in endothelial cells under I/R injury, several drugs or approaches have been developed.…”

Physiological stress response of the Wistar albino rats orally exposed to polystyrene nanoparticles

“…Compared to the negative control and tris (2-chloroethy) phosphate (TCEP) alone, the binary mixture of PS-MPs and TCEP in that study induced the lowest activity in mice (Mus musculus). Rodent studies, however, have demonstrated alterations in SOD activity due to engineered nanoparticles exposure early in life or in adulthood [40,66,67]. Likewise, in the intestine of male marine medaka (Oryzias melastigma), chronic exposure to PS particles (10 µm) led to increased activity of SOD, while in females its activity was signi cantly decreased in ovaries [68].…”