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Furan (FU) and Cadmium (Cd) are toxic agents, and persistent exposure may harm both human and animal health. Therefore, we explored the effects of FU and Cd on liver of the male rat. Male Wister rat groups are distributed randomly: control group (Cr-water): rats were given DI water; control oil group (Cr-oil): rats received corn oil; Furan group: rats received Furan (FU, 16 mg/kg) orally; Cd group: rats obtain cadmium (Cd, 2 mg/kg) orally; and FU+Cd group: rats given both FU + Cd. For 30 days, each therapy was administered once daily. Blood samples and hepatic tissues were obtained after all rats were euthanized. The outcomes showed that treatment with FU or Cd alone considerably caused liver damage, evidenced by serum increase of AST, ALT, ALP, triglycerides, and cholesterol as well as histological changes. Following FU or Cd exposure, there were significant reductions in CAT, GSH, and SOD contents, as well as increases in malondialdehyde along with upregulated expression of PCNA and TNF-α. In contrast, when FU and Cd were administered together potentiated each other and caused more cellular damage in liver tissue. This study found that the primary modulator for enhancing FU and Cd toxicity when administered together was thought to be oxidative stress pathways. [ABSTRACT FROM AUTHOR]

Furan (FU) is a common food contaminant and environmental pollutant. While cadmium (Cd) is a prevalent environmental contaminant that poses a risk to the health of humans and animals. The goal of the current study was to assess the combined effects of FU and Cd on the kidney of male albino rats. Five groups of rats were designed: Cr-water, Cr-oil, FU (16 mg/kg b.w), Cd (2 mg/kg b.w), and FU+Cd, rats were co-treated with both FU and Cd. All treatments were given orally for 30 days. Renal function testing revealed severe biochemical changes in the rats, indicating substantial tissue injury. In addition, there was a notable rise in malondialdehyde (MDA) levels and a fall in reduced glutathione (GSH) concentration as well as the activity of superoxide dismutase (SOD) and catalase (CAT). Also, prominent histopathological alterations in renal tissues were noticed. Additionally, FU and/or Cd significantly up-regulated the expression profile of Kim-1, and inflammatory markers (TNF-α and iNOS). Meanwhile, Aqp1, and Aqp2 m-RNA genes expression were significantly downregulated along with significant upregulation of apoptotic proteins (PCNA). Intriguingly, the concurrent FU and Cd intoxication elicited additional extensive renal injury than their individual exposure. [ABSTRACT FROM AUTHOR]

Concurrent exposure to antimicrobial and nonsteroidal anti‐inflammatory drugs (NSAIDs) is usually inevitable in most infections and postsurgery. Consequently, the present study was designed to assess the intertwining impact of coadministration of cefepime (CP, a wide spectrum antibiotic) and diclofenac sodium (DF, an NSAID) on rat's liver, kidney, and testes. Rats received saline, CP (180 mg/kg/day, IM), DF (10 mg/kg/day, IM), or a combination of CP and DF. After 14 days, CP or DF induced tissue damage expressed by marked biochemical alterations in hepatic and renal function tests. Besides this, disrupted lipid metabolism and testosterone levels along with significant histological changes in hepatic, renal, and testicular tissues were noticed. A significant increase in malondialdehyde and decreases in superoxide dismutase and catalase activities alongside significant upregulated caspase 3 expression in tissues following CP or DF treatment suggested a bearable influence of oxidative stress, lipid peroxidation, and cell death. Accordingly, the simultaneous therapy of CP and DF evoked more obvious tissue damage than their individual treatment. Overall, data concluded that concurrent use of CP and DF in medical practice is a worrisome matter, so it should be done cautiously to avoid synergistic deleterious outcomes. [ABSTRACT FROM AUTHOR]