article · Canadian Journal of Physiology and Pharmacology
Exposure to aluminium oxide nanoparticles causes marked cardiotoxic effects in rat models. Daily administration over fourteen days disrupted heart electrical activity, seen through altered electrocardiogram readings, and increased serum indicators of cardiac damage including lactate dehydrogenase, creatine phosphokinase, and CK-MB. The nanoparticles also worsened lipid profiles by raising triglycerides, total cholesterol, and low-density lipoprotein while lowering high-density lipoprotein. Within heart tissue, nanoparticle exposure triggered oxidative stress, marked by elevated malondialdehyde and depleted protective enzymes such as superoxide dismutase, catalase, and glutathione. Levels of inflammatory markers including tumour necrosis factor-alpha and nitric oxide rose, whereas connexin 43 expression fell. Pretreatment with gallic acid taken orally for fourteen days before nanoparticle administration significantly counteracted these adverse effects, improving electrical activity, antioxidant defences, and tissue health, although nitric oxide levels remained unaltered.
Nanomaterials are widely used across manufacturing and consumer industries, raising concerns about involuntary exposure and organ toxicity. Demonstrating that aluminium oxide nanoparticles disrupt heart rhythms, tissue integrity, and lipid regulation highlights clear health risks. Showing that gallic acid counters these toxic effects offers insights into protective mechanisms and potential interventions against nanoparticle-induced cardiovascular damage.
This research represents early-stage preclinical work identifying gallic acid as a possible protective agent against nanomaterial-induced cardiotoxicity. Potential applications include dietary supplements or protective therapeutics for workers in industries with high nanoparticle exposure. However, the findings are restricted to a fourteen-day rodent model, meaning real-world applications remain distant and will require extensive formulation development, pharmacokinetic studies, and human clinical trials.
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The objectives of present study were to examine the effects of aluminum oxide (Al2O3) nanoparticles on myocardial functions, electrical activities, morphology, inflammation, redox state, and myocardial expression of connexin 43 (Cx43) and the effect of gallic acid (GA) on these effects in a rat animal model. Forty male albino rats were divided into 4 equal groups: the control (normal) group; the Al2O3 group, rats received Al2O3 (30 mg·kg(-1), i.p.) daily for 14 days; the nano-alumina group, rats received nano-alumina (30 mg·kg(-1), i.p.) daily for 14 days; and the nano-alumina + GA group, rats received GA (100 mg·kg(-1) orally once daily) for 14 days before nano-alumina administration. The results showed disturbed ECG variables and significant increases in serum levels of LDH, creatine phosphokinase (CPK), CK-MB, triglycerides (TGs), cholesterol and LDL, nitric oxide (NO), and TNF-α and myocardial concentrations of NO, TNF-α, and malondialdehyde (MDA), with significant decreases in serum HDL and myocardial GSH, SOD, catalase (CAT), and Cx43 expression in the nano-alumina group. Pretreatment with GA improved significantly all parameters except serum and myocardial NO. We concluded that chronic administration of Al2O3 NPs caused myocardial dysfunctions, and pretreatment with GA ameliorates myocardial injury induced by nano-alumina, probably through its hypolipidaemic, anti-inflammatory, and antioxidant effects and upregulation of Cx43 in heart.
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DOI: 10.1139/cjpp-2015-0446
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