scholarly journals Assessment of Immunotoxicity and Oxidative Stress Induced by Zinc Selenium/Zinc Sulphide Quantum Dots

2021 ◽  
Vol 2 ◽  
Author(s):  
V. G. Reshma ◽  
P. V. Mohanan
Keyword(s):  
Oxidative Stress ◽  
Quantum Dots ◽  
Cell Death ◽  
Zinc Sulphide ◽  
Ros Production ◽  
Dna Ladder ◽  
Griess Reagent ◽  
Swiss Albino Mice ◽  
Albino Mice

Although ZnSe/ZnS quantum dots (QDs) have emerged as apparently less hazardous substitute to cadmium-based QDs, their toxicity has not been fully understood. Huge levels of ROS production and associated difficulties comprise the underlying reason for nanomaterial toxicity in cells. This will cause both immunotoxicity and genotoxicity. In the current work, Zinc Selenium/Zinc Sulphide (ZnSe/ZnS) QDs was synthesized, characterized and analyzed for its role in oxidative stress induction in two cell lines (HepG2 and HEK) and Swiss Albino mice. ROS production and influence of catalase activity in ROS production measured by DCFHDA assay in both HepG2 and HEK cells after exposure to ZnSe/ZnS QDs. Assessment of nitrile radical formation carried out by griess reagent. Level of GSH is assessed as a marker for oxidative stress induced by QDs. Cell death induced after exposure to ZnSe/ZnS QDs investigated by Calcein AM-PI live dead assay. Apoptotic DNA ladder assay carried out for studying the potential of ZnSe/ZnS QDs to induce DNA fragmentation. In vivo bio-nano interaction was studied by exposing Swiss Albino mice to ZnSe/ZnS QDs via i.v. and i.p. injection. Antioxidant assays were carried out in brain and liver homogenates to study the oxidative stress. LPO, GSH, GPx, GR and SOD are considered as biomarkers for the stress analysis. Blood brain barrier (BBB) integrity also studied. Spleenocytes proliferation assay was carried out to study the immunotoxicity response. ZnSe/ZnS QDs do not induce visible oxidative stress upto a concentration of 50 μg/ml. Cell death occurs at higher concentration (100 μg/ml) caused by ROS production. Overall study apparently provide attentive information that ZnSe/ZnS QDs is not capable of eliciting any serious damages to liver and brain tissues which in turn substantiates its applicability in biomedical applications.

scholarly journals S-Methylcysteine (SMC) Ameliorates Intestinal, Hepatic, and Splenic Damage Induced by Cryptosporidium parvum Infection Via Targeting Inflammatory Modulators and Oxidative Stress in Swiss Albino Mice

Biomedicines ◽  
2020 ◽  
Vol 8 (10) ◽  
pp. 423
Author(s):  
Ehab Kotb Elmahallawy ◽  
Gehad E. Elshopakey ◽  
Amira A. Saleh ◽  
Ahmad Agil ◽  
Ahmed El-Morsey ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Histopathological Examination ◽  
Intestinal Parasites ◽  
Untreated Group ◽  
High Dose ◽  
Dependent Manner ◽  
Swiss Albino Mice ◽  
Albino Mice ◽  
Dose Dependent

Cryptosporidiosis has been proposed to be one of the major causes of diarrhoeal disease in humans worldwide that possesses zoonotic concern. Thereby, this study investigated the potential effects of s-Methylcysteine (SMC) on the parasite in vivo followed by the measurement of cytokines, oxidative stress parameters, and an investigation of the major histopathological changes. Sixty male Swiss albino mice weighing 20–25 g were allocated equally into five groups and orally administered saline only (control), SMC only (SMC50) (50 mg/kg b.w.), and 104Cryptosporidium parvum oocysts per mouse via an esophageal tube (C + ve untreated). The fourth and fifth groups (C + SMC25, C + SMC50) administrated 104C. parvum oocysts combined with SMC25 (low dose) and 50 (high dose) mg/kg b.w., respectively. At days 7 and 14 post-infection (PI), the feces was collected from each group in order to count C. parvum oocysts. After two weeks of treatment, the animals were euthanized and the serum was collected for biochemical analysis. Next, the intestinal, spleen, and liver sections were dissected for histopathological examination. The results revealed lower oocyst numbers in the C + SMC25 and C + SMC50 groups compared to the infected untreated group. Moreover, higher doses of SMC treatment significantly reduced the enteritis induced by C. parvum in a dose-dependent manner. The hepatic lesions were also mitigated as demonstrated in C + SMC25 and C + SMC50 groups unlike the infected group via lowering the serum alanine aminotransferase (ALT), aspartate aminotransferase (AST), and alkaline phosphatase (ALP) enzymes and increasing albumin and globulin serum levels. SMC administration also reduced cytokines production (SAP, TNF-α, IL-6, and IFN-γ) mediated by Cryptosporidium infection in contrast to the infected untreated group. There were marked lymphoid depletion and amyloidosis observed in the infected untreated group, while the treated groups showed obvious increase in the lymphoid elements. Moreover, the scoring of intestinal parasites, hepatic, and splenic lesions in the SMC-treated groups exhibited significantly lower pathological lesions in different organs in a dose-dependent manner, compared to the infected untreated group. Our results also revealed a significant change in the malondialdehyde content with an elevation of glutathione and superoxide dismutase in the intestines collected from C + SMC25 and C + SMC50 mice relative to the untreated group. Taken together, our results indicated that SMC could be a promising effective compound for treating and declining C. parvum infestation via restoring structural alterations in different tissues, enhancing antioxidant enzymes, and suppressing the cytokines liberation.

Glial cytotoxicity of low doses of cadmium as a model of heavy metal pollution influence on vertebrates

2020 ◽  
Vol 31 (1) ◽  
pp. 3-10
Author(s):  
V. S. Nedzvetsky ◽  
V. Ya. Gasso ◽  
A. M. Hahut ◽  
I. A. Hasso
Keyword(s):  
Oxidative Stress ◽  
Cell Death ◽  
Programmed Cell Death ◽  
Oxidative Damage ◽  
Cadmium Chloride ◽  
Glioma Cells ◽  
Low Doses ◽  
Genotoxic Effects ◽  
Cadmium Ions

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.

Ameliorating effects of white mulberry on iron-overload-induced oxidative stress and liver fibrosis in Swiss albino mice

2021 ◽  
pp. 112520
Author(s):  
Anil Khushalrao Shendge ◽  
Sourav Panja ◽  
Tapasree Basu ◽  
Nikhil Baban Ghate ◽  
Nripendranath Mandal
Keyword(s):  
Oxidative Stress ◽  
Liver Fibrosis ◽  
Iron Overload ◽  
Swiss Albino Mice ◽  
Albino Mice ◽  
White Mulberry
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