Effect of Immune Booster on Cardiac Oxidative Marker in Lead Exposed Male Wistar Rats

Lead is one of the most causes of environmental toxicants and a major health concern due to its toxic effects on vital organs, particularly the heart, liver, kidneys, and nervous system. Exposing to lead, even at low concentrations, has been associated with increased oxidative stress, lipid peroxidation, and depletion of essential antioxidant enzymes, which may predispose individuals to cardiovascular dysfunctions. Presently, attention has been drawn to the potential role of natural immune boosters and antioxidant supplements in mitigating oxidative the damage caused by the environmental toxins like lead. That is why we designed to evaluate the Effect of Immune Booster on Cardiac Oxidative Marker in Lead-Exposed Male Wistar Rats with the aim of determining the antioxidant and cardioprotective potential of the immune booster.
A total of twelve healthy adult male Wistar rats weighing between 120–150 g was used for this study. The rats were randomly assigned into four experimental groups, each containing three rats: Group 1 (Control) received distilled water only; Group 2 (Immune Booster) received the immune booster without lead exposure; Group 3 (Lead) received lead acetate to induce toxicity; and Group 4 (Lead + Immune Booster) received both lead acetate and immune booster. Lead acetate was administered orally at a dose sufficient to induce oxidative stress, while the immune booster was given at a therapeutic dose recommended for a period of 21 days. At the end of the treatment, blood and cardiac tissues were collected for biochemical analysis.

Cardiac oxidative markers such as malondialdehyde (MDA), glutathione (GSH), superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), and glutathione S-transferase (GST) were measured using standard spectrophotometric methods. Body weights and heart weights were also weighed and recorded. The results obtained were analyzed using the Statistical Package for Social Sciences (SPSS), and differences between groups were assessed using t-test and one-way ANOVA at a significance level of p < 0.05.
The research study revealed that lead exposure elevated MDA levels, indicating increased lipid peroxidation and oxidative damage in cardiac tissues. There was also a significant reduction in the activities of antioxidant enzymes (GSH, SOD, CAT, GPx, and GST) in the lead-exposed rats compared to the control group, suggesting that lead toxicity compromises the antioxidant defense system. However, rats that received both lead and the immune booster showed remarkable improvement in antioxidant enzyme activities and a significant reduction in MDA levels. This implies that the immune booster effectively restored balance by neutralizing free radicals and enhancing endogenous antioxidant capacity.
In addition, administration of the immune booster alone led to improved biochemical indices and body weight gain compared to the control, demonstrating its potential role in maintaining physiological balance and supporting cardiac function. The combined treatment (lead and immune booster) group exhibited values closer to the control group, confirming the protective effect of the immune booster against lead-induced oxidative stress. Overall, the immune booster significantly improved oxidative markers, minimized lipid peroxidation, and maintained cellular integrity in the heart tissue of lead-exposed rats.
In conclusion, this study established that the immune booster possesses strong antioxidant and cardioprotective properties capable of fighting the oxidative stress induced by lead exposure. It can be inferred that regular supplementation with immune boosters rich in antioxidants could serve as a preventive and therapeutic strategy against heavy metal-induced cardiac toxicity. This suggests potential benefits in promoting cardiovascular health and protecting individuals at risk of environmental lead exposure. Further studies involving molecular and histological assessments are recommended to explore the mechanisms underlying these protective effects and to validate their applicability in human health.