Curcuma reduces kidney and liver damage induced by titanium dioxide nanoparticles in male Wistar rats.

Objective: The current study was designed to investigate the protective effects of curcuma caplet against titanium dioxide nanoparticles (nTiO2)-induced damage in liver and kidney of male Wistar rats. Materials and Methods: Thirty adult (7-8 week old) male rats (200 g) were randomly divided into 5 groups of 6 each. The first and second groups received olive oil and nTiO2 (300 mg/kg body weight) as control and nTiO2 groups, respectively. The third, fourth, and fifth groups received Curcuma at concentrations of 100, 200, and 300 mg/kg body weight in addition to 300 mg/kg body weight of nTiO2, respectively. The treatment was performed through gavage for 3 weeks. Rats' blood was examined for total antioxidant capacity (TAC), total oxidant status (TOS), and malondialdehyde (MDA) levels as well as antioxidant enzymes superoxide dismutase (SOD), and glutathione peroxidase (GPx), and activity of liver enzymes alanine transaminase (ALT), aspartate transaminase (AST), alkaline phosphatase (ALP), lactate dehydrogenase (LDH), and renal factors (urea, uric acid, and creatinine). Histological analyses were also performed to estimate the extent of hepatic and renal injury. Results: nTiO2-induced liver and kidney damage by decreased serum SOD, GPx, and TAC (p<0.05). Fu +rthermore, nTiO2 increased serum MDA and TOS, and renal (Creatinine, Urea and Uric acid) and liver parameters (ALT, AST, ALP and LDH) (p<0.05). However, Curcuma treatment was able to moderate these changes dramatically (p<0.05). The results were confirmed by histopathological data. Conclusion: This study showed the antioxidant properties of curcuma against the side effects of nTiO2.

Role of Cerium Oxide Nanoparticles in a Paraquat-Induced Model of Oxidative Stress: Emergence of Neuroprotective Results in the Brain.

Paraquat (PQ), as a widely used herbicide, enhances the formation of free radicals and oxidative stress. Cerium oxide nanoparticles (CeNPs) are one of the most utilized and effective nanoparticles having strong antioxidative properties and inhibiting free radicals. Here, we aimed to investigate the effects of CeNPs on brain oxidative toxic stress injury induced with PQ. The male rats were treated intraperitoneally daily with PQ (50 mg/kg/day) and CeNPs (15, 30, and 60 mg/kg/day) alone or in combination for 2 weeks. After treatments, the brain tissue samples were collected. Oxidative toxic stress biomarkers including lipid peroxidation (LPO), total antioxidant capacity (TAC), and total thiol molecules (TTM) as well as DNA damage and caspase-3 levels were measured. Moreover, the mRNA expression levels of Nestin and Neurod1 were assayed. Our results showed that PQ has significantly increased brain LPO, DNA damage, and caspase-3 levels and further reduced TAC and TTM contents, as well as expression levels of Nestin and Neurod1, compared with the control group (injection of saline). CeNPs (15- and 30-mg/kg doses) in groups co-administered with PQ significantly ameliorated the LPO, DNA damage, and caspase-3 levels while increasing TAC and TTM contents as well as enhancing Nestin and Neurod1 mRNA expression levels in the brain samples (P < 0.05). These findings suggest a neuroprotective and antioxidant role for CeNPs in PQ-induced brain injury. However, further studies are required to clarify its clinical/pharmacological significance.