Moudhi Almutlaq

Oxidative stress (OS) plays an important role in the pathology of certain human diseases. Scientists have developed great interest regarding the determination of oxidative stress caused after the administration of nano-graphene composites (PEG-nGO). Graphene oxide sheets (GOS) were synthesized via a modified Hummer's method and were characterized by X-ray diffraction (XRD), ultraviolet-visible spectroscopy (UV), and transmission electron microscopy (TEM). The method of Zhang was adopted for cracking of GOS. Then nano-graphene oxide was PEGylated with polyethylene glycol (PEG). PEGylation of nGO was confirmed by Fourier-transform infrared spectroscopy (FTIR), UV spectroscopy and TEM. The average size distribution of nGO and PEG-nGO was determined by using dynamic light scattering (DLS). Subsequently, an in vivo study measuring a marker for oxidative stress, namely lipid peroxides, as well as antioxidant agents, including catalase, superoxide dismutase, glutathione, and glutathione S-transferase was conducted. A comparison at different intervals of time after the administration of a dose (5 mg/kg) of PEG-nGO was carried out. An increase in free radicals and a decrease in free radical scavenging enzymes in organs were observed. Our results indicated that the treatment with PEG-nGO caused an increased OS to the organs in the first few hours of treatment. However, the liver completely recovered from the OS after 4 h. Brain, heart and kidneys showed an increased OS even after 4 h. In conclusion increased OS induced by PEG-nGO could be detrimental to brain, heart and kidneys.

Abstract Seaweeds are a group of marine multicellular algae; the presence of antioxidant phytochemical constituents in Seaweed Chaetomorpha sp . extracts has received attention for their role in the prevention of human diseases. This study explores the phytochemical constituents, antioxidant, and anticancer properties of the Cladophoraceae, Chaetomorpha sp . Energy dispersive x-ray spectroscopy (EDX), and Gas chromatography-mass spectrometry (GC/MS) were performed to study the chemical structure and chemical formula. Different concentrations of ethanol and aqueous extracts of Chaetomorpha were used to estimate antioxidant activity by 2,2-diphenyl-1-picrylhydrazyl (DPPH) radical scavenging activity and total flavonoid, phenolic, and tannins content assays. Anti-tumor activity against breast cancer cell lines (MCF-7 and MDA-MB-231) was assessed by 3-(4,5-Dimethylthiazol-2-cyl)-2,5-Diphenyltetrazolium Bromide (MTT) assay. The EDX analysis indicated the presence of oxygen, silicon, and calcium as dominant elements. Antioxidant assays indicated that the ethanol extracts of Chaetomorpha consisted of a total of 189.14 ± 0.99 mg QE/g flavonoid content, 21.92 ± 0.43 mg GAE/g phenolic content and 21.81 ± 0.04 mg GAE/g tannins content. The DPPH radical scavenging assay exhibited higher antioxidant activity IC 50 (9.41 ± 0.54 mg/mL) in the ethanol extract. Moreover, it showed high anticancer activity by growth inhibition in the MDA-MB-231 breast cancer cell line and low IC 50 (225.18 ± 0.61 µg/mL). GC/MS analysis revealed the presence of Dichloracetic acid (DCA) as the active antitumor constituent of Chaetomorpha sp .; other anticancer compounds identified were Oximes and L-α-Terpinol. The results revealed that the type of Chaetomorpha sp . studied here possesses very unique and novel constituents and active potent antitumor chemical constituents and it can act as a promising antioxidant and anticancer agent for future applications in pharmaceutical industries.

The Renin Angiotensin System (RAS) is a hormonal system that is responsible for blood pressure hemostasis and electrolyte balance. It is implicated in cancer hallmarks because it is expressed locally in almost all of the body's tissues. In this review, current knowledge on the effect of local RAS in the common types of cancer such as breast, lung, liver, prostate and skin cancer is summarised. The mechanisms by which RAS components could increase or decrease cancer activity are also discussed. In addition to the former, this review explores how the administration of AT1R blockers and ACE inhibitors drugs intervene with cancer therapy and contribute to the outcomes of cancer.

Background: Alzheimer disease is a progressive neurodegenerative disease, affecting a very high proportion of the aging population. Several studies have demonstrated that one of the main contributors to this disease is oxidative stress (OS), which causes peroxidation of protein, lipids, and DNA resulting in the formation of advanced glycosylated end products (AGE) in the brain tissues. These AGE are usually associated with the amyloid β (Aβ), which could further aggravate its toxicity and its clearance. Antioxidants counteract the deterioration caused by OS. Objective: We aimed to evaluate the effect of vitamin D3 and curcumin on primary cortical neuronal cultures exposed to Aβ 1-42 toxicity for different time periods. Methods: Primary cortical neuronal cultures were set up and exposed to Aβ 1-42 for up to 72 hours. Cell viability was studied by 3[4,5-dimethylthiazole-2-yl]-2,5-dipheyltetrazolium bromide (MTT) and lactate dehydrogenase (LDH) assay. Biochemical assays for OS such as lipid peroxidation, reduced Glutathione(GSH), Glutathione S-transferase (GST), catalase, and superoxide dismutase (SOD) were conducted. Sandwich enzyme-linked immunosorbent assay (ELISA) was used to study the neurotrophic growth factor (NGF) expression. Results: Treatments with Aβ 1-42 caused an elevation in lipid peroxidation products, which were ameliorated in the presence of vitamin D3 and curcumin. Both enzymatic (GST, catalase, and SOD) and nonenzymatic antioxidants (reduced GSH) were raised significantly in the presence of vitamin D3 and curcumin, which resulted in the better recovery of neuronal cells from Aβ 1-42 treatment. Treatment with vitamin D3 and curcumin also resulted in the upregulation of NGF levels. Conclusions: This study suggests that vitamin D3 and curcumin can be a promising natural therapy for the treatment of Alzheimer disease.

In the current COVID-19 pandemic, severe acute respiratory syndrome coronavirus 2 uses angiotensin-converting enzyme-2 (ACE-2) receptors for cell entry, leading to ACE-2 dysfunction and downregulation, which disturb the balance between the classical and counter-regulatory renin-angiotensin system (RAS) in favor of the classical RAS. RAS dysregulation is one of the major characteristics of several cardiovascular diseases; thus, adjustment of this system is the main therapeutic target. RAS inhibitors-particularly angiotensin-converting enzyme inhibitors (ACEIs) and angiotensin II type 1 receptor blockers (ARBs)-are commonly used for treatment of hypertension and cardiovascular disease. Patients with cardiovascular diseases are the group most commonly seen among those with COVID-19 comorbidity. At the beginning of this pandemic, a dilemma occurred regarding the use of ACEIs and ARBs, potentially aggravating cardiovascular and pulmonary dysfunction in COVID-19 patients. Urgent clinical trials from different countries and hospitals reported that there is no association between RAS inhibitor treatment and COVID-19 infection or comorbidity complication. Nevertheless, the disturbance of the RAS that is associated with COVID-19 infection and the potential treatment targeting this area have yet to be resolved. In this review, the link between the dysregulation of classical RAS and counter-regulatory RAS activities in COVID-19 patients with cardiovascular metabolic diseases is investigated. In addition, the latest findings based on ACEI and ARB administration and ACE-2 availability in relation to COVID-19, which may provide a better understanding of the RAS contribution to COVID-19 pathology, are discussed, as they are of the utmost importance amid the current pandemic.