Menadione perturbs oxidative stress biomarkers and testicular function indices of rats.

In this study, we evaluated the influence of menadione on the androgenic, oxidative stress biomarkers, and testicular function indices in rats. Rats (20) were randomized into four groups (A-D) of five rats each. Rats in groups A, B, C, and D received the vehicle of administration (olive oil), 25, 50, or 100 mg/kg body weight menadione intraperitoneally, respectively, for 7 days. Menadione lowered serum cholesterol, follicle-stimulating hormone, luteinizing hormone, and testosterone and luteinizing hormone reduced significantly in rats when compared with the control rats. Furthermore, menadione lowered the testicular function indices in the testes of rats. The activities of superoxide dismutase and catalase in the testes of menadione-treated rats decreased significantly. Also, glutathione was depleted with concomitant malondialdehyde increase. The findings of this study show that menadione induces testicular toxicity by depleting the antioxidant defense system leading to perturbation in the testicular function indices.

Lophirones B and C halt acetaminophen hepatotoxicity by upregulating redox transcription factor Nrf-2 through Akt, PI3K, and PKC pathways.

We investigated the mechanism of lophirones B- and C-mediated protection against acetaminophen hepatotoxicity. Mice were pretreated with 20 mg/kg body weight lophirones B and C for 7 days and challenged with acetaminophen on day 7. Acetaminophen raised nuclear factor-κB (NF-κB) in the liver of mice but lowered protein kinase B (Akt). Although, acetaminophen produced no significant alteration on nuclear erythroid related factor-2 (Nrf-2), phosphoinositide 3-kinase (PI3K) and protein kinase C (PKC), lophirones B and C raised the level of these proteins and Akt. The acetaminophen-mediated increase in NF-κB was significantly reversed by lophirones B and C. Lophirones B and C prevented acetaminophen-mediated alterations in serum biomarkers of hepatic injury. Similarly, lophirones B and C lowered the biomarkers of oxidative stress in the liver of acetaminophen-treated mice. It can be inferred from this study that lophirones B and C prevent acetaminophen-induced liver injury by enhancing Nrf-2 through Akt, PI3K, and PKC pathways.

Involvement of oxidative stress in protocatechuic acid-mediated bacterial lethality.

The involvement of oxidative stress in protocatechuic acid-mediated bacterial lethality was investigated. Minimum inhibitory concentrations (MIC) and minimum bactericidal concentration (MBC) of protocatechuic acid against Escherichia coli, Pseudomonas aeruginosa, and Staphylococcus aureus are 600 and 700 µg/ml, 600 and 800 µg/ml, and 600 and 800 µg/ml, respectively. The optical densities and colony-forming units of protocatechuic acid-treated bacteria decreased in time-dependent manner. Protocatechuic acid (4× MIC) significantly increased the superoxide anion content of E. coli, P. aeruginosa, and S. aureus compared to dimethyl sulfoxide (DMSO). Superoxide dismutase, catalase, and NAD+ /NADH in protocatechuic acid-treated E. coli, P. aeruginosa, and S. aureus increased significantly when compared to DMSO. Conversely, level of reduced glutathione decreased in protocatechuic acid-treated E. coli, P. aeruginosa, and S. aureus, while glutathione disulfide increased when compared to DMSO. Furthermore, malondialdehyde and fragmented DNA increased significantly following exposure to protocatechuic acid. Protocatechuic acid inhibited the activity of complexes I and II. From the above findings, protocatechuic acid enhanced the generation of reactive oxygen species (superoxide anion radical and hydroxyl radical) in E. coli, P. aeruginosa, and S. aureus, possibly by autoxidation, fenton chemistry, and inhibiting electron transport chain resulting in lipid peroxidation and DNA fragmentation and consequentially bacterial cell death.