The abundant use of lead (Pb; toxic heavy metal) worldwide has increased occupational and ecosystem exposure, with subsequent negative health effects. The flavonoid luteolin (LUT) found in many natural foodstuffs possesses antioxidant and anti-inflammatory properties. Herein, we hypothesized that LUT could mitigate liver damage induced by exposure to lead acetate (PbAc). Male Wistar rats were allocated to four groups: control group received normal saline, LUT-treated group (50 mg/kg, oral, daily), PbAc-treated group (20 mg/kg, i.p., daily), and LUT+PbAc-treated group (received the aforementioned doses via the respective routes of administration); the rats were treated for 7 days. The results revealed that PbAc exposure significantly increased hepatic Pb residue and serum activities of aspartate aminotransferase (AST), alanine aminotransferase (ALT), and total bilirubin value. Oxidative reactions were observed in the liver tissue following PbAc intoxication, characterized by the depletion and downregulation of antioxidant proteins (glutathione, glutathione reductase, glutathione peroxidase, superoxide dismutase, catalase, nuclear factor erythroid 2-related factor 2, and heme oxygenase-1), and an increase in oxidants (malondialdehyde and nitric oxide). Additionally, PbAc increased the release and expression of the pro-inflammatory cytokines (tumor necrosis factor alpha and interleukin-1 beta), inducible nitric oxide synthase, and nuclear factor kappa B. Moreover, PbAc enhanced hepatocyte loss by increasing the expression of pro-apoptotic proteins (Bax and caspase-3) and downregulating the anti-apoptotic protein (Bcl-2). The changes in the aforementioned parameters were further confirmed by noticeable histopathological lesions. LUT supplementation significantly reversed all of the tested parameters in comparison with the PbAc-exposed group. In conclusion, our findings describe the potential mechanisms involved in the alleviation of PbAc-induced liver injury by luteolin via its potent anti-inflammatory, antioxidant, and anti-apoptotic properties.

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Natural antibacterial agents such as citrox are effective against many foodborne pathogens and foods contaminated with bacteria. We studied the antimicrobial effects of citrox solutions (1% and 2%) on the total viable counts of methicillin-resistant Staphylococcus aureus (MRSA) in chicken meat fillets. The total coliform group counts found in the chicken samples were also determined. The samples were treated with S. aureus at a concentration of 10⁶ colony-forming units (cfu)/g of meat and vacuum-packed (VP) at 4 °C for 3, 6, 9, 12, 15, 18, and 21 days. We also studied the effect of citrox on the total volatile basic nitrogen (TVBN) content and pH changes during the storage period of the meat samples. The results revealed that citrox inhibited the growth of MRSA in the chicken fillets. The total viable counts of MRSA decreased after treatment with 2% citrox in all treated samples that were stored at 4 °C by approximately 2 log units compared with the samples inoculated with S. aureus (Chicken-Staph groups) after 3, 6, 9, and 12 days of storage, and by approximately 1 log unit compared with the control samples treated with salt (Chicken-Salt groups) after 3, 6, and 9 days of storage. TVBN was reduced in the Chicken-Citrox-treated samples stored at 4 °C compared with the Chicken-Staph- and Chicken-Salt-treated samples. The results indicated that citrox is effective in reducing the total counts of MRSA and in improving the quality of chicken during the first three days of storage by reducing the number of bacteria by 1 log unit and extending the shelf life of chicken.