There is a persistent need to look for alternative therapeutic modalities to help control the pandemic of antimicrobial resistance. Assessment of antibacterial and anti-biofilm effects of vitamin C (ascorbic acid) was the aim of the current study. The micro-dilution method determined the minimal inhibitory concentration (MIC) of ascorbic acid or antibiotics alone and in combinations against Pseudomonas aeruginosa (P. aeruginosa) clinical isolates. The micro-titer plate method monitored the effect of ascorbic acid on the biofilm-producing isolates of P. aeruginosa. The effect of ascorbic acid on the differential expression of different antibiotic-resistant genes and biofilm encoding genes of P. aeruginosa isolates were also tested using real-time polymerase chain reaction (PCR). For in vivo assessment of the antibacterial effects of ascorbic acid alone or combined with an antibiotic, rats were infected with P. aeruginosa clinical isolate followed by different treatment regimens. MICs of ascorbic acid among P. aeruginosa isolates were in the range of 156.2–1,250 μg/ml, while MIC50 and MIC90 were 312.5 and 625 μg/ml, respectively. At sub-inhibitory concentrations (19.5–312.5 μg/ml), ascorbic acid had 100% biofilm inhibitory effect. Furthermore, ascorbic acid-treated bacteria showed downregulation of genes underpinning biofilm formation and antibiotic resistance. In vivo assessment of vitamin C and ceftazidime in rats showed that administration of both at a lower dose for treatment of pseudomonas infection in rats had a synergistic and more powerful effect. Vitamin C shows excellent in vitro results as an antibacterial and anti-biofilm agent. Vitamin C should be routinely prescribed with antibiotics to treat bacterial infections in the clinical setting.
Cisplatin (CP) and doxorubicin (DX) can cause testicular injury by inducing oxidative/nitrosative stress, inflammation, and apoptosis, Naringenin (NG) has antioxidant, antinitrative, anti-inflammatory, and anti-apoptotic effects. This study investigated the potential ability of NG to block gonadotoxicity induced CP and DX in male rats. The rats received one injection of either CP (10 mg/kg, i.p.) or DX (15 mg/kg, i.p.), and treated with NG (50 mg/kg/day, p.o.) for 10 days beginning 6 days prior to CP and DX administration. NG significantly prevented the decreases of serum testosterone and inhibin B in rats received CP and DX. Additionally, NG significantly decreased the elevated testicular malondialdehyde, tumor necrosis factor-α/interleukin-10 ratio, and caspase-3 in CP- and DX-treated rats. NG also significantly raised the decreased testicular Bcl-2/Bax ratio, and total antioxidant status in CP- and DX-challenged rats. In addition, NG significantly increased P-glycoprotein level in testes of rats received CP and DX. Moreover, NG significantly decreased the testicular histopathological injury, and immunohistochemical expression of inducible nitric oxide synthase induced by CP and DX in rat testes. It was concluded that NG impeded gonadotoxicity of CP and DX in male rats by mitigating oxidative stress, nitrosative stress, inflammation, and apoptosis.
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