Mustard seeds since ancient times have been used by mankind for its culinary, as well as medicinal, properties. Mustard preparations are well known for their mildly laxative, diuretic, and calming effect on the liver bile. It has crucial contents of polyphenolic and phenolic compounds). Family Brassicaceae, is popularly known as Indian mustard, has both therapeutic and edible qualities. Considering the unappreciated side effects of chemically modified agents and the limited capacity of the modified pharmaceutical product to regulate major diseases, it is important to recognize new medicinal structures from other naturally occurring sources, including plant kingdom sources. Usually, in normal circumstances, these metabolites are detoxified by conjugating with antioxidative defense system (glutathione), but TAA toxic metabolites overwhelm the detoxification process and lead to a change in cell membrane permeability, disturb mitochondrial activity leading to lipid peroxidation, which contributes to the release of, cytokines, and prostaglandins Thus, in initiating severe liver toxicity, the reactive oxygen species (ROS) may be the maestro by secreting a range of pro-inflammatory factors that could hurt DNA. TAA toxicity is triggered by its reactive metabolite sulfene or sulfone via the CYP450 system, which affects the most internal vital activities and causes oxidative stress and glutathione (GSH) depletion.
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TAA toxicity results from a series of biotransformation into toxic metabolites that takes place in cytochrome P-450 enzymes in the liver. Thioacetamide C2H5NS/TAA is an organosulfur compound known to induce acute or chronic liver disease (fibrosis and cirrhosis) in the experimental animal model very similar to that happen in humans. The liver is one of the most important organs responsible for the process of metabolism and selective uptake and clearance of drugs xenobiotic and environmental toxins, the matter which makes it very sensitive to drug toxicity.
Mustard introduced a protective and medicinal effect against TAA in both its forms. DNA genotoxicity was significantly reversed. The expression levels of TNF-α and IL-6 in serum and tissue were markedly downregulated. In addition, nanoforms of mustard ethanol extract have notably increased the levels of GSH, SOD and significantly reduced the levels of MDA. The antioxidant content of Phenolic acids, flavonoids in mustard ethanolic extract substantially decreased the levels of ALT, AST, ALP and rehabilitated the histopathological alterations. DNA genotoxicity and hepatic pathology, and immunohistologic (IHC) changes were assayed. The levels of serum liver functions, total cholesterol (TCHo), total glyceride (TG), total bilirubin (TBIL), hepatic malonaldhyde (MDA) and nitric oxide (NO),glutathione (GSH), sodium oxide dismutase (SOD), as well as tumor necrosis factor (TNF-α,) and interleukin 6 (IL-6), were estimated. To induce liver failure, male rats were injected with 350 mg/kg bw TAA IP, then treated orally with a dose of 100 mg/kg for 15 d of mustard extract and its nanoform before and following induction.
Mustard ethanolic extract was analyzed by HPLC/MS. The purpose of this study was to investigate whether mustard in its normal or nanoparticles could confer a protective/therapeutic effect against TAA-induced acute liver failure in experimental animal models. Detoxification is one of the main vital tasks performed by the liver.
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