## 4 Discussion  
Plants synthesize aromatic substances such as phenols or their oxygenated derivatives. Most of these are recognized as flavoring compounds, while some herbs and spices that are typically used to season food also carry compounds that hold medicinal value. Generally, extracts that have high phenolic content exhibit good antioxidant activity. Our results suggest that _Carum carvi_ possesses strong potential to inhibit oxidative stress-induced lipid peroxidation and in vitro DNA damage. Our results were also in accordance with the DPPH-scavenging property of _Carum carvi_, indicating the manifestation of potent antioxidant activity [27]. Another significant indicator of antioxidant potential lies in the plant extract's reducing capacity [28]. _Carum carvi_ extract transformed the Fe\({}^{3+}\)/ferricyanide complex to a ferrous state. _Carum carvi_ extract was found to have a dose-dependent increase in reducing power at concentrations between 20 and 100 \(\upmu\)L/ml. In cases of paracetamol overdose, a toxic metabolic product, i.e., N-acetyl-p-benzo-quinone-imine (NAPQI), is produced and metabolized via CYP 450 [29]. This highly reactive byproduct in turn alkylates and oxidizes intracellular GSH, resulting in GSH depletion in the liver, which ultimately leads to increased peroxid oxidative activity. Elevation in peroxidation of lipids results in disruption of mitochondrial and nuclear functions, leading to oxidative stress [30]. Any agent that has the potential to suppress the levels of CYP 450 can protect the tissues from the deleterious effect of acetaminophen toxicity, such as depletion in reduced glutathione and peroxidation of membrane lipids, leading to cellular toxicity. Lipid peroxidation, measured by MDA formation is an important marker to study cellular toxicity. It has been observed that enzymes such as QR and GST may promote resistance to hepatotoxicity induced by acetaminophen [31]. We observed that acetaminophen toxicity led to lipid  
Figure 7: Liver histopathological architecture of rats treated with _Carum carvi_. Representative micrographs (original magnification: 40\(\times\)) showing alterations in liver histopathology by acetaminophen and normalization of the anatomical architecture by _Carum carvi_ treatment. Arrows represent diffuse vacuolation and infiltration of mononuclear inflammatory cells. (**A**) Control group. (**B**) Acetaminophen-treated group. (**C**) Acetaminophen + _Carum carvi_ (100 mg/kg). (**D**) Acetaminophen + _Carum carvi_ (200 mg/kg). (**E**) Only _Carum carvi_ (200 mg/kg). peroxidation, resulting in the membrane destabilization of hepatocytes, which in turn resulted in the depletion of phase II enzymes produced by hepatocytes. In the present study, we observed that GST levels were depleted by the acetaminophen administration to rats, which may have been due to the damage caused by acetaminophen on the liver cells, resulting in the poor functioning of hepatocytes. However, high levels of oxidative species production during acetaminophen toxicity can attack biological macromolecules, leading to peroxidation of lipids and exhaustion of antioxidant enzymes (CAT, GPx, etc.) and, thus, resulting in further stressed conditions. In cells with excessive oxidative stress, the levels of xanthine oxidase (a non-cytochrome oxidative enzyme) are significantly higher, resulting from the interaction of cellular macromolecules with free radicals. It has been observed that xanthine oxidase is actively involved in the metabolism of acetaminophen. In determining liver toxicity induced by acetaminophen, elevated activities of xanthine oxidase have been reported [32]. Thus, depletion of antioxidant enzymes could be the result of a decrease in glutathione content caused by acetaminophen toxicity [33]. A significant increase in enzymatic activities was observed when the animals were treated with _Carum carvi_, thus indicating protection against acetaminophen-induced liver toxicity by upregulation of the antioxidant defense system in liver cells.