Rats that were given lycopene, both alone and in combination with exposure to cadmium, showed normal behavioral activity and food intake when compared to the untreated control rats. In contrast, rats that were exposed to cadmium without lycopene treatment displayed a decrease in activity and food intake starting from third week of the experiment compared to the control rats. No deaths were reported in any of the experimental groups.
The blood cadmium level in control rats was measured at 0.0024±0.0001 ppm, which significantly increased (
P<0.05) in rats exposed to cadmium (0.573±0.018 ppm). Blood cadmium levels were comparatively lower in rats exposed to cadmium and received lycopene (0.217±0.016 ppm) than in cadmium-exposed rats.
Table (1) shows the estimated hematological parameters in rats that received lycopene, rats exposed to cadmium and rats exposed to cadmium and administered with lycopene compared to the control rats.
Tables (2) (a, b, c) shows the biochemical parameters (serum levels) in rats that received lycopene, rats exposed to cadmium and rats exposed to cadmium and lycopene compared to the control rats.
Table (3) shows the levels of total thiols, glutathione, catalase, glutathione peroxidase, superoxide dismutase, TAC, H
2O
2, MDA in the liver and kidney homogenates of rats that received lycopene, rats exposed to cadmium and rats exposed to cadmium and lycopene compared to the control rats.
The toxic effects of cadmium include the oxidation of cell membrane lipids, which significantly reduces the production of ATP and glutathione in the mitochondria. Additionally, cadmium toxicity impairs the function of antioxidant enzymes, thereby exacerbating existing oxidative stress. Ultimately, cadmium-induced toxicity leads to apoptosis due to the activation of the caspase cascade
(Kawata et al., 2018).
Indicators of antioxidative status, such as total thiols, glutathione, superoxide dismutase, glutathione peroxidase, catalase and total antioxidant capacity, were remarkably decreased in rats exposed to cadmium. It is postulated that the generated ROS in the course of cadmium toxicity caused oxidation of these endogenous antioxidants and consequently dramatically suppressed their capacity to overcome the resultant oxidative damage.
Glutathione and catalase are among the endogenous antioxidants that work directly to eradicate free radicals
(Liu et al., 2018). Oxidation of these antioxidants leads to the accumulation of free radicals and exacerbation of oxidative stress. Catalase decomposes hydrogen peroxide (H
2O
2), which accounts for lipid peroxidation. Inhibited catalase activity allows hydrogen peroxide to induce severe oxidizing effects in rats. H
2O
2 action is the base of the Fenton reaction, which generates the highly oxidizing hydroxyl radical (OH)
(Shi et al., 2024).
The present significant increase in the levels of malondialdehyde (MDA) in cadmium-intoxicated rats is ascribed to lipid peroxidation of the cell membranes. MDA, being a marker of lipid peroxidation, is one of the consequences of oxidative damage
(Wang et al., 2018; Shamsi et al., 2020).The antioxidant activity of lycopene is related to its scavenging of free radicals as evidenced by its direct action to eliminate H
2O
2, NO and hydroxyl OH radicals and its capability to inhibit lipid peroxidation
(Ilhane et al., 2022; Juan et al., 2021).
Lycopene down-regulates gene expression of iNOS, decreases NO level and increases tissue glutathione (GSH) (
Leh and Lee, 2022;
Grabowska et al., 2019; Kiran et al., 2023). In addition, it prevents oxidative stress-induced apoptosis
(Francenia et al., 2019). Under the circumstances of oxidative stress, Lycopene elevates the total antioxidant status. Lycopene could enhance the activities of all antioxidant enzymes including catalase, superoxide dismutase and glutathione peroxidase and inhibit oxidative enzymes (
Bin-Jumah et al., 2022;
Świątkiewicz et al., 2023). It reduces the level of malondialdehyde (MDA) and reduces the synthesis of ROS in general. Lycopene reduces the mitochondrial and intracellular concentrations of ROS. Through these activities, lycopene could protect proteins, DNA and lipids against oxidative damage.
It was concluded that lycopene as a carotenoid could counteract and prevent the progression of the effects of ROS. Lycopene acts through diverse mechanistic pathway to alleviate ROS-induced oxidative damage
(Rejali et al., 2022; Abir et al., 2023).
The present results are in accordance with those of the relevant published studies (
Przybylska, 2020;
Guo et al., 2023) as evidenced by the currently recorded improved levels of antioxidant markers (total thiols, glutathione, catalase and TAC in rats exposed to cadmium and had access to Lycopene. These findings may confirm the positive effect of lycopene on the activity of these antioxidant molecules and consequently reinforcing significant effect on endogenous antioxidant capacity.
The significant decrease in cadmium blood levels in presently cadmium-intoxicated rats and administered lycopene may be interpreted by cadmium chelation. Chelation is one of the postulated roles of lycopene to mitigate the damaging effects induced by chemical toxins
(Nadeem et al., 2019; Hedayati et al., 2019). Cadmium is the trigger of oxidative overload and decreasing its level in the blood greatly limiting the initiation of oxidative stress and thus helps recover the endogenous antioxidant system. The currently assayed haematological and biochemical parameters in rats exposed to cadmium and treated with lycopene revealed improvements toward the control levels. These results may reinforce the proposed synergistic antioxidant role of lycopene in alleviating cadmium-induced oxidative stress.