Abstract
The aim of this study was to evaluate the antioxidant and anti-inflammatory effects of the new [Ru(Q)(Cl)2(H2O)2] complex (RuIII/Q). A new vital complex containing quercetin flavonoid compound (Q) with ruthenium (III) ions was synthesized. The molar conductivity of the RuIII/Q complex was measured in dimethylsulfoxide (DMSO) with value 12 (Ω−1 mol−1 cm−1, indicating their non-electrolytic nature. Infrared (FTIR) spectroscopic investigation of the RuIII/Q complex indicated that Q is coordinated as a bidentate with Ru metal ions through the oxygen of carbonyl C(4)=O group and oxygen of phenolic C(3)−O group based on the wavenumber shifts at 1654 and 1335 cm−1 respectively. The electronic (UV−Vis) spectra and the magnetic susceptibility value (1.85 B.M.) revealed that the Ru(III) complex has an octahedral geometry. The average diameter of the RuIII/Q nanoparticles was approximately 7–15 nm according to the transmission electron microscopy. The thermogravimetric study (TG/DTG) indicates that the RuIII/Q compound is quite stable until 300 °C. To assess biological activity, 60 male rats were allocated to six groups, namely control, DG (D-galactose), Q, RuIII/Q, DG plus Q, and DG plus RuIII/Q. Antioxidant enzymes (SOD, CAT, GPx, and GRx), markers of lipid peroxidation (such as MDA), expression of genes (namely Nrf2, Cu-ZnSOD, CAT, GPx, cyto c, P53, Bax, BCl2, caspase-3, and caspase-9 in testicular tissue), glutamate, 4-hydroxynonenal (HNE), GSH, HCY, amyloid beta, and GABA levels were evaluated in brain tissues. Cytokines, such as IL-6 and TNF-α, histological and ultrastructural studies were estimated in both the brain and testicular tissues, while the comet assay was performed in the brain tissue. RuIII/Q administration either alone or combined with DG reduced oxidative injury to normal levels and decreased apoptotic activities. Thus, RuIII/Q inhibited injury in both the testis and brain and reduced oxidative stress in male rats. The (RuIII/Q) complex has a potent ameliorative effect against aging neurotoxicity, reproductive toxicity, and antihepatic cancer activity induced by D-galactose (DG).
Highlights
Observed molar conductance (12 (Ω−1 mol−1 cm−1 ) of the RuIII complex in DMSO for 10−3 M solution at 25 ◦ C is consistent with the non-electrolytic nature of the complex [57]
Recent evidence suggests that oxidative stress plays a vital role in inducing aging and polyphenols act as antioxidant agents and reduce the risk of neurodegenerative diseases
The results demonstrate that DG induced severe neuroinflammation with appearance of irregular and discontinuous myelinated sheath and large area of hemorrhage, testicular damage with appearance of pyknotic nuclei and reduction in speramtogenc layers, more Geneotoxicity with large tail length in the commet assay and more viable HepG2.The novel RuIII /Q complex alleviated oxidative injury and cytotoxicity induced by DG
Summary
Antioxidant enzymes (SOD, CAT, GPx, and GRx), markers of lipid peroxidation (such as MDA), expression of genes (namely Nrf, Cu-ZnSOD, CAT, GPx, cyto c, P53, Bax, BCl2, caspase-3, and caspase-9 in testicular tissue), glutamate, 4-hydroxynonenal (HNE), GSH, HCY, amyloid beta, and GABA levels were evaluated in brain tissues. Cytokines, such as IL-6 and TNF-α, histological and ultrastructural studies were estimated in both the brain and testicular tissues, while the comet assay was performed in the brain tissue. Studies have shown that D-galactose (DG) treatment causes oxidative injury and mitochondrial dysfunction in male mice and rats [1].
Sign-in/Register to view highlights & summary 
Published Version (
Free)
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call