Abstract
The current study investigated the protective potential of Azolla pinnate ethanolic extract (APE) against lead-induced hepatotoxicity in rats. Sixty male Wistar albino rats were randomly allocated into six groups (n = 10). The control group was orally administrated with saline. The second group received lead acetate (100 mg/kg body weight (BW) orally for 60 days). The third group was fed with APE (10 mg/kg BW orally for 60 days). The fourth group was administrated with lead acetate like the second group and APE like the third group, concomitantly, for 60 days. The fifth group was administrated with APE like the third group for 30 days, then orally administrated with the lead acetate like the second group for another 30 days. The sixth group was administrated with lead acetate like the second group for 30 days, then with APE like the third group for a further 30 days. Phytochemical analysis of APE indicated the presence of peonidin 3-O-glucoside cation, vitexin, rutin, thiamine, choline, tamarixetin, hyperoside, astragalin, and quercetin. The latter has been elucidated using one- and two-dimensional nuclear magnetic resonance (1D and 2D NMR) and liquid chromatography–mass spectrometry (LC–MS-MS). Lead acetate increased the serum levels of alanine and aspartate aminotransferases and that of urea, creatinine, tumor necrosis factor alpha, and interleukin 1β, hepatic tissue malondialdehyde contents, and caspase 3 protein expression, as well as altering the hepatic tissue architecture. However, it decreased the serum levels of interleukin 10 and glutathione (GSH) contents, and the activities of catalase and superoxide dismutase in hepatic tissue. In contrast, the administration of APE ameliorated the lead-induced alterations in liver function and structure, exemplifying the benefits of Azolla’s phytochemical contents. Collectively, A. pinnate extract is a protective and curative agent against lead-induced hepatotoxicity via its antioxidant, anti-inflammatory, and anti-apoptotic impacts.
Highlights
The main cause of hepatotoxicity in all living organisms is exposure to heavy metals, toxins, drugs, or harmful compounds, including carbon tetrachloride, sodium oxalate, and ethylene glycol [1]
The 1H-Nuclear Magnetic Resonanse (NMR) spectra of A. pinnata ethanolic extract showed a dominance of signals in the aliphatic region
The intoxication of rats with lead acetate in the current study decreased the serum level of the anti-inflammatory cytokine interleukin 10 (IL-10) (Table 4). This finding was consistent with that of [62,63], who indicated that exposure to lead acetate decreases IL-10 in the rats’ cerebral cortex, confirming the role of leadership in the development of an inflammatory response in rat brain tissue [62]. Such a decrease in IL-10 due to lead acetate exposure may be implicated in the increased serum levels of IL-1β and the promotion of inflammatory signals, as it was shown that IL-10 can block IL-1β gene expression [64]
Summary
The main cause of hepatotoxicity in all living organisms is exposure to heavy metals, toxins, drugs, or harmful compounds, including carbon tetrachloride, sodium oxalate, and ethylene glycol [1]. Lead acetate induces experimental hepatic injury in rats via the induction of oxidative stress following an imbalance between free radical generation and the antioxidant defense system [6]. This oxidative stress leads to the generation of reactive oxygen species (ROS), including the hydroperoxides, singlet oxygen, and hydrogen peroxide, resulting in serious damage to different biomolecules, i.e., DNA, enzymes, proteins, and membrane lipids. Chronic lead toxicity results in short-term memory loss, nausea, depression, loss of coordination, numbness and tingling in the extremities, and abdominal pain [16], in addition to anemia [14]. Lead toxicity harms both adults and children [17]
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