Synthesis and Evaluation of In-vitro and In-vivo Antioxidant Properties: Novel 2-phenyl-3-Sustituted Quinazoline-4-ones | Chapter 5 | Recent Developments in Chemistry and Biochemistry Research Vol. 7

 

Quinazolinones, a prominent scaffold in medicinal chemistry, exhibits a wide array of biological activities. This research focused on synthesizing and evaluating two series of 3-substituted quinazolin-4(3H)-ones for their antioxidant properties. The evaluation encompassed both in vitro methods, namely DPPH and reducing power method, and in vivo studies using lipid peroxidation, superoxide dismutase (SOD), catalase, glutathione reductase, and glutathione peroxidase assays on erythrocytes of carbon tetrachloride-intoxicated rats. The objective was to establish structure-antioxidant activity relationships based on diverse substituents at position 3 of the quinazolinone scaffold. The newly synthesized quinazoline derivatives, designated as 7a1-7a8 and 7b1-7b8, displayed notable antioxidant properties, potentially contributing to their observed biological activity. Among the two series, compound 7b5, bearing a methyl piperazine at the 3rd position and a chlorine atom at the 6th position on the 3-substituted quinazoline nucleus, exhibited outstanding antioxidant activity in both in vitro and in vivo methods. Furthermore, compounds 7a5 and 7a8 demonstrated significant antioxidant properties in the DPPH assay, while compounds 7a3, 7a4, 7a5, and 7a8 displayed notable activity in the reducing power method. In vivo studies revealed significant antioxidant properties in compounds 7a5, 7a8, 7b4, 7b6, and 7b8. Additionally, compounds 7a6 and 7b7 showed promising antioxidant activity in vivo. These findings underscore the potential of quinazoline-based compounds as therapeutic agents for managing oxidative stress-related disorders.

 

Author (s) Details

Praveen Kumar Kusuma
Department of Pharmaceutical Chemistry, School of Pharmaceutical Sciences, Delhi Pharmaceutical Sciences and Research University, New Delhi-110017, India.

 

Girijasastry Vedula
Department of Pharmaceutical Sciences, College of Pharmacy, Andhra University, Visakhapatnam – 530003, India.

 

Please see the book here:- https://doi.org/10.9734/bpi/rdcbr/v7/2769

 

Toxicity Preventive Potential of Anti-Inflammatory CeO2 Nanoparticles in HUVE Cells | Chapter 8 | Recent Trends in Chemical and Material Sciences Vol.7

The mechanism behind cerium oxide nanoparticles' (CeO2 NPs) cytoprotective capability against cytotoxic nitric oxide (NO) donors and H2O2 is currently unknown. The lipopolysaccharide (LPS)-induced cytokines IL-1 and TNF- were dramatically reduced by CeO2 NPs that had been synthesised and described. Because NP-induced ROS/NO did not cause toxicity in HUVE cells, the main goal of this investigation was to determine the capacities of CeO2 NPs in terms of signalling effects that could have happened owing to reactive oxygen species (ROS) and/or NO. Two NO-donors were used in conjunction with CeO2 NPs in human umbilical vein-derived endothelial (HUVE) cells to achieve this goal. To our knowledge, there has been little investigation on CeO2 NPs' modulatory ability against known NO-donors. SNP (sodium nitroprusside, #ab145732 from Abcam plc, Cambridge, UK) and DETA-NO (Z)-1-[N-(2-Aminoethyl)-N-(2-ammonioethyl)amino]diazen-1-ium-1,2-diolate or DETA-NONOate #ab144627 from Abcam plc, Cambridge, UK) were the two NO donors utilised in this The IC50s of two NO donors (DETA-NO; 1250 110 M and sodium nitroprusside (SNP; 950 89 M) as well as the IC50 of H2O2 (120 7 M) were used to assess cytoprotective capacity and its underlying mechanism. Total ROS (as a collective marker of hydrogen peroxide, superoxide radical, hydroxyl radical, and other ROS) was assessed using DCFH-DA, and significant ROS was deciphered using a specialised probe DHE. The data demonstrated that signalling processes mediated primarily by and/or NO are responsible for CeO2 NPs at 100 g/mL ameliorating toxicity. The fact that NP exposure had no effect on mitochondrial membrane potential (MMP) and that CeO2 NPs-mediated recovery of MMP loss caused by exogenous NO donors and H2O2 suggested that NP-mediated generation was extra-mitochondrial. The mechanism behind the NP-induced gain in GSH and persistent cytoplasmic ROS is partially explained by data on activated glutathione reductase (GR) and unchanged glutathione peroxidase (GPx) activity. Instead of being inhibited by CeO2 NP administration, cells may develop the ability to tolerate exogenously generated toxicity due to increased antioxidant capacity due to non-cytotoxic ROS and/or NO generation.

Author(s) Details:

Mohd Javed Akhtar,
King Abdullah Institute for Nanotechnology, King Saud University, Riyadh-11451, Saudi Arabia.


Maqusood Ahamed,
King Abdullah Institute for Nanotechnology, King Saud University, Riyadh-11451, Saudi Arabia.

Please see the link here: https://stm.bookpi.org/RTCAMS-V7/article/view/6101

Is Atmospheric Superoxide Essential? Accelerated Death of Animals in a Quasi-Neutral Electric Atmosphere | Chapter 6 | Emerging Challenges in Environment and Earth Science Vol. 1

 The goal of the research was to investigate the biological effect of micromolar quantities of ionised gases by removing them from inhaled air via electrostatic removal („air ion deprivation"). A morphological investigation of the adeno- and neurohypophysis was done due to the possible involvement of these structures in the physiological reactions to inhaled air ions (AI), particularly micromolar levels of gas-phase superoxide.

The electrostatic field created by acrylic glass surfaces was used to deionize ambient air inside an experimental acrylic glass cage (AGC). Four hours after the animals were placed in the AGC, the concentration of negative AIs was not quantifiable, while the concentration of positive ions was (mean SD) 77 18 ions cm-3. In identical silicate glass cages (control), the concentrations of negative and positive AI were 482 128 ionscm-3 and 660 148 ionscm-3, respectively. It has been discovered that a prolonged absence of AI in the ambient air causes animals to die more quickly. The mice and rats which were starved lived 16.2 0.9 and 23.0 1.1 days, respectively. Animal death is significantly linked to neurohormonal regulatory problems and pituitary insufficiency, based on clinical symptoms and ultrastructural changes in the adeno- and neurohypophysis seen in deprived animals. The physiological necessity for AIs and atmospheric superoxide is explored, as well as its involvement in the development of environmental stress in humans, especially premature newborns.

Author(S) Details

Naum Goldstein
Goldstein & Lewin technology GmbH. Dept, of Medical Research. Kastanienweg 23, D-14532 Stahnsdorf, Germany and Latvian Medical Academy. Dzirciema 16. LV-1007, Riga. Latvia.

Tatyana V. Arshavskaya
Latvian Institute for Experimental and Clinical Medicine. O. Vaciesa 4. LV-1004 Riga, Latvia.

View Book:- https://stm.bookpi.org/ECEES-V1/article/view/4702