Humans can be exposed to nanomaterials via a number of routes with the nanoparticles tending to accumulate in vital organs38. From literature, it has been revealed that nanoparticle deposition in vital organs or tissues could induce cellular damage39. A study conducted by Pourmand et al.40 investigated the effects of AgNPs on the body weights of rats. The results showed that AgNPs caused a significant decrease in body weight gain in rats compared to the control group. Similarly, another study by Sharma et al.41 reported a significant decrease in body weight in rats exposed to AgNPs compared to the control group. In this study we evaluated the effects of silver nanoparticles on body weights of male rats. Our results showed dose-dependent decrease on body weight with significant changes at higher doses. Our findings corroborate with Pourmand et al.40 and Sharma et al.41 work suggesting that AgNPs can have toxic effects on the body weight of rats which could be attributed to several factors. One possible explanation is that AgNPs may affect the absorption of nutrients in the gastrointestinal tract, leading to reduced food intake and subsequent weight loss. Another possibility is that AgNPs could directly interfere with the metabolic processes that regulate body weight and energy expenditure, leading to reduced body weight gain. Further studies are needed to determine the mechanisms underlying these effects and to evaluate the potential risks of AgNP exposure in humans.
In this study we investigated the effects of AgNPs on the weight of liver, kidney and heart of male rats. The results showed a significant decrease in the weights of organs in a dose dependent manner, which may be due to the accumulation of AgNPs in these organs. Our findings suggest that AgNPs may induce oxidative stress and inflammation and may cause liver, kidney and heart damage and ultimately alter their respective functions in the body. Previous research work investigated the effects of AgNPs on liver, kidney and heart in male rats which supported our current findings42,43,44.
Major organs in the embryonic stage are extremely susceptible to oxidative stress owing to high metabolic rate45,46 and it is well-known that oxidative stress is a central mechanism of silver nanoparticle toxicity47,48. In this study, biomarkers of oxidative stress and antioxidant systems were measured in the liver, kidney and heart tissues. Lipid peroxidation is a process in which free radicals react with polyunsaturated fatty acids in cell membranes, leading to the production of lipid peroxides. This process can cause damage to cell membranes and other cellular components and disrupt the normal functioning of cells. CAT is an antioxidant enzymes implicated in the cell redox control that aid conversion of hydrogen peroxides to H2O and O249. Glutathione (GSH) on the other hand is a key endogenous non-enzymatic thiol which exerts many biological roles, as well as protection against reactive oxygen and nitrogen species (ROS and RNS)50. Total thiol (T-SH) is a measure of the antioxidant capacity of cells, as thiol-containing molecules such as glutathione play an important role in the maintenance of the cellular redox balance. In this study, our results showed that AgNPs exposure caused a significant increase in the levels of lipid peroxidation products such as malondialdehyde (MDA) in the liver, kidney and heart tissue, indicating oxidative stress. Furthermore, we observed a significant decrease in enzymatic (CAT, SOD) activities and non-enzymatic (GSH) levels, especially at the highest in the liver, heart and kidney. Our results indicate that AgNPs can affect both enzymatic and non-enzymatic components of the antioxidant system in the liver, kidney and heart. In addition, our study showed that AgNP exposure caused a significant decrease in the levels of total thiol in the liver, heart and kidney tissue, indicating a disruption of the antioxidant capacity which can lead to oxidative stress and damage to cellular components in the liver, heart and kidney. Recent studies demonstrated that AgNPs induced oxidative stress and altered the antioxidant system in the liver kidney and heart of male rats51,52,53,54.
Moreover, in this present study treatment of rats with silver nanoparticles caused significant increases in ALT, AST, and ALP levels in the liver compared to control groups, indicating liver damage and suggesting that the toxicity of silver nanoparticles on liver could be due to the production of reactive oxygen species and oxidative stress. A separate study by Srivastava et al.55 reported the potential of AgNPs to affect the activity of transaminase enzymes. Thus, the potential of AgNPs to modulate enzyme activity was accredited to their affinity for thiol groups56,57.
Urea and Creatinine are both waste products that are filtered out of the blood by the kidneys, so changes in their levels can indicate impaired liver and kidney function. The liver plays a vital role in the metabolism of nitrogenous compounds, including the synthesis of urea. Urea is produced in the liver through the urea cycle, a series of biochemical reactions that convert ammonia, a toxic byproduct of protein metabolism, into urea, which is then excreted by the kidneys. The urea cycle takes place primarily in the hepatocytes, the main functional cells of the liver. In this study exposure to silver nanoparticles resulted in a significant increase in urea and creatinine levels in male rats, indicating kidney dysfunction. Our findings suggests that silver nanoparticles have toxic effects on the kidneys of the experimental male rats, as evidenced by increased levels of urea and creatinine. This result corroborates with reports from Mendoza-Magaña et al.58 and Mohammadi et al.59 that treatment with silver nanoparticles caused a significant increase in urea and creatinine levels in male rats compared to control animals.
We investigated the effects of silver nanoparticles on the microscopic structure of liver, kidney, and heart tissues in male rats using H&E staining. Our findings support previous work from which reported that silver nanoparticles caused degenerative changes in liver, kidney and heart tissue of male rats60,61,62,63. The microscopic study from our work showed congestion of central venules, abnormal morphology of hepatocytes with the sinusoids mildly infiltrated by inflammatory cell in liver tissues of the treated group that might be due to lipid peroxidation. These changes may confirm that AgNPs lead to liver damage. Similarly, abnormal glomeruli with abnormal mesengial cells and capsular spaces with interstitial spaces moderately infiltrated by inflammatory cells in kidney tissues of the treated group may further confirm that AgNPs caused kidney damage. Moreover, the congestion of heart tissue with epicardial layer and infiltrating inflammatory cells and macrophages in heart tissues further confirm the damage caused by AgNPs to heart tissues. Taken together, these studies suggest that exposure to silver nanoparticles can cause significant histological changes in liver, kidney, and heart tissues of male rats, which may lead to functional impairment of these organs. Therefore, it is important to carefully evaluate the potential toxic effects of silver nanoparticles on these organs before their use in various biomedical applications.
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