scholarly journals Characteristic Evaluation of Various Formulations of Anti-Aging Cream from Carotenoid Extract of Bacterial Symbiont Virgibacillus salarius Strain 19.PP.Sc1.6

Cosmetics ◽  
2021 ◽  
Vol 8 (4) ◽  
pp. 120
Author(s):  
Lia Kusmita ◽  
NFN Mutmainah ◽  
Agus Sabdono ◽  
Agus Trianto ◽  
Ocky Karna Radjasa ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cell Death ◽  
Protein Denaturation ◽  
Premature Aging ◽  
Water Type ◽  
Oil In Water ◽  
Different Types ◽  
Microbial Symbionts ◽  
Stress Oxidative ◽  
Damage Protein

Premature aging can be triggered by free radicals from UV rays, since exposure to these rays can cause the skin to experience oxidative stress. Oxidative stress induces intracellular DNA damage, protein denaturation, and lipid peroxidation that lead to cell death. However, cell death can be prevented with antioxidants such as carotenoids, which are among the potential natural compounds for its treatment. Sources of carotenoids include microbial symbionts associated with Sinularia sp., one of which is the bacterium Virgibacillus salarius strain 19.PP.Sc1.6, a carotenoid-producing bacteria. This study aims to explore the utilization of carotenoids from the bacterium V. salarius strain 19.PP.Sc1.6 for the preparation of anti-aging creams. Furthermore, the method employed three formulations (vs, ow, and wo) containing different types of cream tested for stability, and antioxidant and sunscreen abilities. The results obtained established that the carotenoid extract from V. salarius strain 19.PP.Sc1.6 was more stable in the cream vs. the oil-in-water type cream with an anionic emulsifier.

scholarly journals Antioxidants Targeting Mitochondrial Oxidative Stress: Promising Neuroprotectants for Epilepsy

2020 ◽  
Vol 2020 ◽  
pp. 1-14
Author(s):  
Nan Yang ◽  
Qi-Wen Guan ◽  
Fang-Hui Chen ◽  
Qin-Xuan Xia ◽  
Xi-Xi Yin ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cell Death ◽  
Brain Activity ◽  
Related Factor ◽  
Mitochondrial Oxidative Stress ◽  
Electrical Brain Activity ◽  
Neuroprotective Strategies ◽  
Cell Death Signaling ◽  
Stress Oxidative

Mitochondria are major sources of reactive oxygen species (ROS) within the cell and are especially vulnerable to oxidative stress. Oxidative damage to mitochondria results in disrupted mitochondrial function and cell death signaling, finally triggering diverse pathologies such as epilepsy, a common neurological disease characterized with aberrant electrical brain activity. Antioxidants are considered as promising neuroprotective strategies for epileptic condition via combating the deleterious effects of excessive ROS production in mitochondria. In this review, we provide a brief discussion of the role of mitochondrial oxidative stress in the pathophysiology of epilepsy and evidences that support neuroprotective roles of antioxidants targeting mitochondrial oxidative stress including mitochondria-targeted antioxidants, polyphenols, vitamins, thiols, and nuclear factor E2-related factor 2 (Nrf2) activators in epilepsy. We point out these antioxidative compounds as effectively protective approaches for improving prognosis. In addition, we specially propose that these antioxidants exert neuroprotection against epileptic impairment possibly by modulating cell death interactions, notably autophagy-apoptosis, and autophagy-ferroptosis crosstalk.

scholarly journals Oil-In-Water Microemulsion Encapsulation of Antagonist Drugs Prevents Renal Ischemia-Reperfusion Injury in Rats

2021 ◽  
Vol 11 (3) ◽  
pp. 1264
Author(s):  
Parisa Hasanein ◽  
Abbas Rahdar ◽  
Mahmood Barani ◽  
Francesco Baino ◽  
Siamak Yari
Keyword(s):  
Oxidative Stress ◽  
Rat Model ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Serum Levels ◽  
Kidney Damage ◽  
Control Group ◽  
Water Type ◽  
Beneficial Effects ◽  
Oil In Water

Developing new therapeutic drugs to prevent ischemia/reperfusion (I/R)-induced renal injuries is highly pursued. Liposomal encapsulation of spironolactone (SP) as a mineralocorticoid antagonist increases dissolution rate, bioavailability and prevents the drug from degradation. In this context, this work develops a new formulation of oil-in-water type microemulsions to enhance the bioavailability of SP. The size of the SP-loaded microemulsion was about 6.0 nm by dynamic light scattering analysis. Briefly, we investigated the effects of nano-encapsulated SP (NESP) on renal oxidative stress, biochemical markers and histopathological changes in a rat model of renal I/R injury. Forty eight male Wistar rats were divided into six groups. Two groups served as control and injury model (I/R). Two groups received “conventional” SP administration (20 mg/kg) and NESP (20 mg/kg), respectively, for two days. The remaining two groups received SP (20 mg/kg) and NESP (20 mg/kg) two days before induction of I/R. At the end of the experiments, serum and kidneys of rats underwent biochemical, molecular and histological examinations. Our results showed that I/R induces renal oxidative stress, abnormal histological features and altered levels of renal biomarkers. Administration of SP in healthy animals did not cause any significant changes in the measured biochemical and histological parameters compared to the control group. However, SP administration in the I/R group caused some corrections in renal injury, although it could not completely restore I/R-induced renal oxidative stress and kidney damage. On the contrary, NESP administration restored kidney oxidative injury via decreasing renal lipid peroxidation and enhancing glutathione, superoxide dismutase and catalase in kidneys of the I/R group. The deviated serum levels of urea, creatinine, total proteins and uric acid were also normalized by NESP administration. Furthermore, NESP protected against renal abnormal histology features induced by I/R. Therefore, NESP has beneficial effects in preventing kidney damage and renal oxidative stress in a rat model of I/R, which deserves further evaluations in the future.

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.

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