## 1 Introduction  
Gentamicin (GTN) is an antibiotic that is widely used to treat severe Gram-negative bacterial infections. This is because of its unique bactericidal and post-antibiotic characteristics coupled with low levels of resistance [1]. However, its clinical use is associated with severe renal injury, imposing a therapeutic limitation [2; 3]. The literature has shown that about 30% of patients treated for more than seven days with GTN showed signs of renal injury [4]. GTN causes oxidative stress, which taxes the nephrons because of the consequent induced inflammation, enhancing the damage [5]; this action culminates in turning on the apoptotic pathway [1]. Abundant evidence shows that oxidative stress induces the production of reactive oxygen species (ROS), which are critical in acute renal injury [6]. This is because ROS, in their interactions, mediate apoptosis by inducing the apoptotic signaling pathway [7]. Several studies have demonstrated the molecular mechanism by which GTN induce renal injury. This is seen to include renal tubular damage leading to necrosis and glomerular congestion, subsequently causing renal dysfunction [8]. Furthermore, reports show that GTN increases serum liver enzymes and induces histological lesions, reflecting its hepatotoxic effects. The pathogenesis of GTN-induced liver toxicity was proposed to be mainly due to inflammation and oxidative stress [9; 10]. Numerous strategies and agents have been employed in an attempt to attenuate the renal toxicity caused by GTN, with limited success [11; 12; 13]. These agents, if scientifically proven to be efficacious and without side effects, could be clinically important in enhancing the safety of GTN. Therefore, reviving the use of this important antibiotic will be of great benefit, particularly on the heels of the increasing antimicrobial resistance and the lack of development of new antibiotics [4]. From this background, and based on the premise that many plants demonstrate hepatoprotective and nephoprotective potential through the prevention of oxidative stress [14; 15; 16], we were encouraged to investigate the protective role of broccoli against GTN-induced nephrotoxicity and hepatotoxicity in rats as a model for drug-induced toxicities. Broccoli (_Brassica oleraca_ L. variety _italica_) (_B. oleraca_) is reported to have a high content of bioactive phytochemicals, such as phenolic compounds, glucosionolates, vitamin C, and mineral nutrients. Additionally, previous studies showed that broccoli extract can exert beneficial effects against chronic diseases of the cardiovascular system and cancer [17]. In addition, numerous reports showed that broccoli prevents oxidative stress, which is implicated in many diseases [18]. Broccoli florets, consumed commonly for their nutritional benefits, have received more attention from researchers. However, the leaves, which have been used as a source of fiber, are now reported to have a much higher content of antioxidants compared to the florets [17]. Thus, the present study aimed to extract, isolate, and identify the contents of broccoli leaf by-product extract (BL) and then to examine the potential benefits of BL against GTN-induced renal and hepatic injury, whereby markers of oxidative stress including, malondialdehydeehyde (MDA), glutathione (GSH), and superoxide dismutase (SOD), were determined in liver and renal samples. Aspartate transaminase (AST), alanine transaminase (ALT), alkaline phosphatase (ALP), creatinine, and urea were assessed. Additionally, to investigate its influence on inflammatory pathways, the mRNA expression levels of tumor necrosis factor alpha (TNF-\(\alpha\)), interleukin-1B (IL-1B), and nuclear factor kappa B (NFkB) were evaluated in liver and kidney tissues.**