Search Results (445)

With the acceleration of the pace of life, increased stress levels, and changes in lifestyle factors such as diet and exercise, the incidence of diseases such as cancer and immunodeficiency has been on the rise, which is closely associated with the impaired antioxidant capacity of the body. Polypeptides and polysaccharides derived from edible fungi demonstrate significant strong antioxidant activity and immunomodulatory effects. Auricularia auricula, the second most cultivated mushroom in China, is not only nutritionally rich but also offers considerable health benefits. In particular, its polysaccharides have been widely recognized for their immunomodulatory activities, while its abundant protein content holds great promise as a raw material for developing immunomodulatory peptides. To meet the demand for high-value utilization of Auricularia auricula resources, this study developed a key technology for the stepwise extraction of polypeptides (AAPP1) and polysaccharides (AAPS3) using a composite enzymatic hydrolysis process. Their antioxidant and immunomodulatory effects were assessed using cyclophosphamide (CTX)-induced immune-suppressed mice. The results showed that both AAPP1 and AAPS3 significantly reversed CTX-induced decreases in thymus and spleen indices (p < 0.05); upregulated serum levels of cytokines (e.g., IL-4, TNF-α) and immunoglobulins (e.g., IgA, IgG); enhanced the activities of hepatic antioxidant enzymes SOD and CAT (p < 0.05); and reduced the content of MDA, a marker of oxidative damage. Intestinal microbiota analysis revealed that these compounds restored CTX-induced reductions in microbial α-diversity, increased the abundance of beneficial bacteria (Paramuribaculum, Prevotella; p < 0.05), decreased the proportion of pro-inflammatory Duncaniella, and reshaped the balance of the Bacteroidota/Firmicutes phyla. This study represents the first instance of synergistic extraction of polypeptides and polysaccharides from Auricularia auricula using a single process. It demonstrates their immune-enhancing effects through multiple mechanisms, including “antioxidation-immune organ repair-intestinal microbiota regulation.” The findings offer a theoretical and technical foundation for the deep processing of Auricularia auricula and the development of functional foods. Full article

Barium chloride (BaCl₂), a known environmental pollutant, induces organ-specific oxidative stress through disruption of redox homeostasis. This study evaluated the protective effects and safety profile of sodium copper chlorophyllin (SCC) and ascorbic acid (ASC) against BaCl₂-induced oxidative damage in the liver and brain of mice using a two-phase experimental protocol. Animals received either SCC (40 mg/kg), ASC (160 mg/kg), or their combination for 14 days prior to BaCl₂ exposure (150 mg/L in drinking water for 7 days), allowing evaluation of both preventive and therapeutic effects. Toxicological and behavioral assessments confirmed the absence of systemic toxicity or neurobehavioral alterations following supplementation. Body weight, liver and kidney indices, and biochemical markers (Aspartate Aminotransferase (ASAT), Alanine Aminotransferase (ALAT), creatinine) remained within physiological ranges, and no anxiogenic or locomotor effects were observed. In the brain, BaCl₂ exposure significantly increased SOD (+49%), CAT (+66%), GPx (+24%), and GSH (+26%) compared to controls, reflecting a robust compensatory antioxidant response. Although lipid peroxidation (MDA) showed a non-significant increase, SCC, ASC, and their combination reduced MDA levels by 42%, 37%, and 55%, respectively. These treatments normalized antioxidant enzyme activities and GSH, indicating an effective neuroprotective effect. In contrast, the liver exhibited a different oxidative profile. BaCl₂ exposure increased MDA levels by 80% and GSH by 34%, with no activation of SOD, CAT, or GPx. Histological analysis revealed extensive hepatocellular necrosis, vacuolization, and inflammatory infiltration. SCC significantly reduced hepatic MDA by 39% and preserved tissue architecture, while ASC alone or combined with SCC exacerbated inflammation and depleted hepatic GSH by 71% and 78%, respectively, relative to BaCl₂-exposed controls. Collectively, these results highlight a differential, organ-specific response to BaCl₂-induced oxidative stress and the therapeutic potential of SCC and ASC. SCC emerged as a safer and more effective agent, particularly in hepatic protection, while both antioxidants demonstrated neuroprotective effects when used individually or in combination. Full article

Reactive oxygen species (ROS) play a dual role as both essential signaling molecules and harmful mediators of damage. Imbalances in the redox state of the liver can overwhelm antioxidant defenses and promote mitochondrial dysfunction, oxidative damage, and inflammation. Complex feedback loops between ROS and immune signaling pathways are a hallmark of pathological liver conditions, such as hepatic ischemia–reperfusion injury (IRI). This is a major cause of liver transplant failure and is of increasing significance due to the increased use of marginally discarded livers for transplantation. This review outlines the major enzymatic and metabolic sources of ROS in hepatic IRI, including mitochondrial reverse electron transport, NADPH oxidases, cytochrome P450 enzymes, and endoplasmic reticulum stress. Hepatocyte injury activates redox feedback loops that initiate immune cascades through DAMP release, toll-like receptor signaling, and cytokine production. Emerging regulatory mechanisms, such as succinate accumulation and cytosolic calcium–CAMKII signaling, further shape oxidative dynamics. Pharmacological therapies and the use of antioxidant and immunomodulatory approaches, including nanoparticles and redox-sensitive therapeutics, are discussed as protective strategies. A deeper understanding of how redox and immune feedback loops interact is an exciting and active area of research that warrants further clinical investigation. Full article

Background/Objectives: Antimicrobial resistance (AMR) is a health related threat world-wide. Biosynthesized gold nanoparticles (AuNPs) using plant extracts have been reported to exhibit certain biological activity. This study aimed to biosynthesize AuNPs using an aqueous extract of Eruca sativa leaves and to evaluate their biocompatibility, antimicrobial activity, and antioxidant properties. Methods: AuNPs were biosynthesized using an aqueous extract of Eruca sativa leaves. Their biocompatibility was evaluated through hemolytic activity and assessments of hepatic and renal functions in rats. AuNPs were biologically evaluated as antimicrobial and antioxidant agents. Results: The AuNPs exhibited particle sizes of 27.78 nm (XRD) and 69.41 nm (AFM). Hemolysis assays on red blood cells revealed negligible hemolytic activity (<1%). Hepatic enzyme levels, including alanine aminotransferase (ALT), aspartate aminotransferase (AST), alkaline phosphatase (ALP), and lactate dehydrogenase (LDH) were studied. ALT, AST, and ALP levels showed no significant changes compared to the negative control. However, LDH levels were elevated at higher concentration (52.8 µg/mL), while the lower concentration (26.4 µg/mL) appeared to be safer. Renal biomarkers, urea and creatinine, showed no significant changes at either concentration, indicating minimal nephrotoxicity. The antimicrobial activity of AuNPs, plant extract, and gold salt was tested against five microorganisms: two Gram-positive bacteria (Staphylococcus aureus, Streptococcus pneumoniae), two Gram-negative bacteria (Escherichia coli, Pseudomonas aeruginosa), and a fungal strain (Candida albicans). The AuNPs exhibited minimum inhibition concentrations (MICs) of 13.2 µg/mL against S. aureus and S. pneumoniae, 26.4 µg/mL against E. coli and C. albicans, and 39.6 µg/mL against P. aeruginosa, suggesting selectivity towards Gram-positive bacteria. Furthermore, the AuNPs demonstrated strong antioxidant activity, surpassing that of vitamin C. Conclusions: The biosynthesized AuNPs exhibited promising biocompatibility, selective antimicrobial properties, and potent antioxidant activity, supporting their potential application in combating the AMR. Full article

Volatile organic compounds (VOCs) are highly volatile chemicals in natural and anthropogenic environments, significantly affecting indoor air quality. Major sources of indoor VOCs include emissions from building materials, furnishings, and consumer products. Natural wood products release VOCs, including terpenes and aldehydes, which exert diverse health effects ranging from mild respiratory irritation to severe outcomes, such as formaldehyde-induced carcinogenicity. The temporal dynamics of VOC emissions were investigated, and the toxicological and physiological effects of the VOCs emitted by two types of natural wood, Korean Red Pine (Pinus densiflora) and Japanese Cypress (Chamaecyparis obtusa), were evaluated. Using female C57BL/6 mice as an animal model, the exposure setups included phytoncides, formaldehyde, and intact wood samples over short- and long-term durations. The exposure effects were assessed using oxidative stress markers, antioxidant enzyme activity, hepatic and renal biomarkers, and inflammatory cytokine profiles. Long-term exposure to Korean Red Pine and Japanese Cypress wood VOCs did not induce significant pathological changes. Japanese Cypress exhibited more distinct benefits, including enhanced oxidative stress mitigation, reduced systemic toxicity, and lower pro-inflammatory cytokine levels compared to the negative control group, attributable to its more favorable VOC emission profile. These findings highlight the potential health and environmental benefits of natural wood VOCs and offer valuable insights for optimizing timber use, improving indoor air quality, and informing public health policies. Full article

Acetaminophen (APAP) overdose is a major cause of drug-induced liver injury (DILI) globally, which necessitates effective therapies. Gallic acid (GA), a naturally abundant polyphenol, possesses potent antioxidant and anti-inflammatory properties that may overcome the limitations of N-acetylcysteine (NAC), such as its narrow therapeutic window. This study systematically investigated the hepatoprotective effects and underlying molecular mechanisms of GA against APAP-induced acute liver injury (ALI). Mice received an intraperitoneal injection of APAP (300 mg/kg), followed by an oral administration of GA (50 or 100 mg/kg) or NAC (150 mg/kg) 1 h post-intoxication. Both GA and NAC significantly ameliorated hypertrophy and histopathological damage, as evidenced by reduced serum ALT/AST levels and inflammatory cytokines. TUNEL staining revealed a marked suppression of apoptotic and necrotic cell death, further supported by the downregulation of pro-apoptotic Bax and the upregulation of anti-apoptotic Bcl-2 mRNA expression. GA and NAC treatment restored hepatic glutathione (GSH) content, enhanced antioxidant enzyme gene expression, and reduced malondialdehyde (MDA) accumulation. Mechanistically, GA and NAC inhibited MAPK phosphorylation while activating AMPK signaling. Taken together, these findings demonstrate that GA mitigates APAP-induced ALI by modulating oxidative stress and inflammation through the regulation of MAPK/AMPK signaling proteins. Full article

Bothus podas (wide-eyed flounder) is a benthic flatfish likely exposed to microplastic (MP) pollution. We investigated MP ingestion and associated physiological effects in wild B. podas collected from Mallorca (Balearic Islands), Spain. Markers of oxidative stress, detoxification, and immunity were quantified in intestinal, hepatic, and splenic tissues. MPs were observed in the gastrointestinal tracts of 87.5% of the 24 specimens analyzed, with an average of 3.8 ± 0.6 items per fish. Fiber-type MPs predominated in both the gastrointestinal tract (69.6%) and sediment samples (97%). Additionally, micro-Fourier transform infrared spectroscopy analysis confirmed that the majority of ingested MPs were composed of polyethylene, polypropylene, and polyester. Fish were categorized into low (<3 items) and high (≥3 items) MP groups based on the median number of plastic items found in the gastrointestinal tract to assess sublethal impacts. In the gut, high-MP fish exhibited significantly elevated activities of detoxification enzymes: ethoxyresorufin-O-deethylase (phase I) and glutathione s-transferase (phase II), along with increased antioxidant enzyme superoxide dismutase and inflammatory myeloperoxidase. Gut catalase and malondialdehyde (MDA) were not significantly different between groups. In liver tissues, no biomarkers differed significantly with MP exposure. In the spleen, lysozyme and alkaline phosphatase activities were significantly higher in high-MP fish, while splenic MDA remained unchanged. These results indicate that gastrointestinal MP exposure triggers local oxidative stress responses and systemic immune activation in B. podas. Overall, ingestion of environmentally relevant MP levels elicited detoxification and inflammatory responses without significant increases in MDA, an indicator of oxidative damage, highlighting the physiological stress imposed by plastic pollution on benthic fish. Full article

The objective of this study was to formulate a compound suspension comprising paeoniflorin and curcumin, assess its quality characteristics, and investigate its protective efficacy against acute liver injury in mice. The prescriptions were screened using a single-factor test, and nine groups of suspensions were prepared using the dispersion method. Fifty KM mice (four weeks old) were selected and randomly divided into five groups: the CON, LD, PF, CUR, and PC groups. The doses of both paeoniflorin and curcumin were 100 mg/kg BW, and different suspensions were given to different groups by gavage for 14 days. All the groups except the CON group were injected intraperitoneally with 20 μg/kg LPS and 700 mg/kg D-GalN on the last day. According to the results, the suspension prepared using the optimal prescriptions was orange-yellow in color, with homogeneous turbidity and good re-dispersibility. The combination treatment could reduce the severity of pathological injuries of liver, improve the ultrastructure of hepatocytes, increase the activities of T-SOD, GSH-Px, and CAT, decrease the levels of IFN-γ, TNF-α, and IL-1, and down-regulate the expression of genes such as TLR4, MyD88, IκBα, and NLRP3. The underlying mechanism might be associated with the enhancement of antioxidant enzyme activities, inhibition of the TLR4/NF-κB/NLRP3 signaling pathway, and suppression of inflammasome assembly and release in hepatic tissues. Full article

Plywood and particle boards, commonly used in construction and interior environments, are sources of indoor chemical emissions from synthetic adhesives, resins, and surface treatments. Among these, formaldehyde, classified as a group 1 carcinogen by the International Agency for Research on Cancer, and other compounds are associated with oxidative stress, inflammation, and organ toxicity. This study aimed to evaluate the toxicological and physiological effects of plywood and particleboard emissions in female C57BL/6 mice. The mice were exposed to formaldehyde, phytoncides, and untreated wood samples under short- (30–60 days) and long-term (120–180 days) conditions. Biological effects were assessed through histopathology of major organs, differential white blood cell counts, oxidative stress markers, antioxidant enzyme activities (catalase and glutathione peroxidase), liver and kidney function tests (alanine aminotransferase, aspartate aminotransferase, blood urea nitrogen, and creatinine), and inflammatory cytokine profiling (interferon-gamma, tumor necrosis factor-α, interleukin (IL)-10, and IL-12p70). These findings revealed no significant pathological changes or systemic toxicity following long-term exposure. Minor elevations in hepatic and renal biomarkers were observed but remained within physiological limits. Antioxidant responses and cytokine fluctuations suggested mild adaptive and immunomodulatory effects. These results highlight the importance of reducing emissions from engineered wood products to improve indoor air quality and minimize potential health risks. Full article

Chinese perch (Siniperca chuatsi), an economically important freshwater fish in China, faces ammonia nitrogen stress under high-density aquaculture. This study investigated chronic ammonia nitrogen exposure effects on juvenile fish (95 ± 5 g) to establish safe concentration. Acute toxicity tests revealed a 96 h-LC₅₀ of 12.91 mg/L ammonia nitrogen, with a safe concentration of 1.29 mg/L ammonia nitrogen (non-ionic ammonia: 0.097 mg/L). In 28-day chronic experiments with ammonia nitrogen levels at 0, 0.61, 1.29, and 2.58 mg/L, ammonia nitrogen induced hepatic oxidative stress, with total superoxide dismutase, catalase, and glutathione peroxidase activities and malondialdehyde content increasing proportionally to ammonia nitrogen concentration initially but declining over time. Concurrently, gill Na⁺-K⁺-ATPase activity was significantly suppressed, while the gene expression of ammonia transporters (rhag, rhbg, and rhcg) exhibited ammonia nitrogen concentration-dependent upregulation, inversely correlated with the exposure duration. Histological gill damage intensified at higher concentrations. Hepatic ammonia detoxification enzymes activities (asparagine synthase, glutamine synthetase, and glutamate dehydrogenase) and glutamine accumulation increased with ammonia nitrogen levels, aligning with gene expression trends, though enzyme activity diminished over time. Serum alanine aminotransferase and aspartate aminotransferase activities and their gene expressions rose with ammonia nitrogen levels, while total protein declined. These findings demonstrate that chronic ammonia nitrogen stress disrupts antioxidant capacity, osmoregulation, and nitrogen metabolism, compelling Chinese perch to mitigate toxicity via glutamine synthesis. To ensure sustainable aquaculture, ammonia nitrogen levels should remain below 1.29 mg/L under adequate dissolved oxygen conditions. Full article

Background: Curcumin, a bioactive polyphenol derived from turmeric, has demonstrated potential therapeutic effects in metabolic dysfunction-associated steatotic liver disease (MASLD) by modulating inflammation, oxidative stress, hepatic fat accumulation, and fibrosis. Objective: To evaluate the efficacy of curcumin in reducing hepatic steatosis and liver stiffness in patients with MASLD. Methods: In this randomized, double-blind, placebo-controlled trial, 78 patients with type 2 diabetes mellitus (T2DM) and MASLD were randomly assigned to receive either curcumin (1500 mg/day) or placebo for 12 months. The primary outcome was the change in tumor necrosis factor (TNF) levels. Secondary outcomes included changes in interleukin-1 beta (IL-1β), interleukin-6 (IL-6), antioxidant enzyme activities (glutathione peroxidase, superoxide dismutase), the oxidative stress marker malondialdehyde, non-esterified fatty acids, and hepatic parameters (hepatic steatosis and liver stiffness). Assessments were conducted at baseline and at 3, 6, 9, and 12 months. Results: All participants completed the study (curcumin group: n = 39; placebo group: n = 39). Curcumin significantly reduced TNF levels at all follow-up points compared to placebo (p < 0.001). IL-1β, IL-6, and malondialdehyde levels also declined significantly (p < 0.001), while antioxidant enzyme activities, including glutathione peroxidase and superoxide dismutase, increased significantly (p < 0.001), indicating improved oxidative balance. Furthermore, curcumin led to significant reductions in non-esterified fatty acids, total body fat, BMI, hepatic steatosis, and liver stiffness compared to placebo. Conclusions: Twelve months of curcumin supplementation improved glycemic control, reduced systemic inflammation and oxidative stress, and significantly improved hepatic steatosis and liver stiffness in patients with MASLD. These findings support curcumin as a promising adjunctive therapy for MASLD management. Full article

Soy protein isolate (SPI) is a high-purity protein from defatted soybeans, providing emulsifying and gelling functions for plant-based foods and supplements. Hydrolysis can facilitate the production of bioactive small-molecule proteins or peptides with potential functional applications. In this study, 20% hydrolyzed soy protein (20% HSP) was prepared from SPI, and the effects of 20% HSP and SPI on alleviating oxidative stress in Caenorhabditis elegans (C. elegans) and regulating immune–gut microbiota in cyclophosphamide (CTX)-induced immunocompromised BALB/c mice were investigated. In C. elegans, both SPI and 20% HSP (300 μg/mL) enhanced locomotive activities, including body bending and head thrashing, and improved oxidative stress resistance under high glucose conditions. This improvement was mediated by increased antioxidant enzyme activities (SOD, CAT, and GSH-Px), while malondialdehyde (MDA) content was reduced by 60.15% and 82.28%, respectively. Both of them can also significantly extend the lifespan of normal C. elegans and paraquat-induced oxidative stress models by inhibiting lipofuscin accumulation. This effect was mediated through upregulation of daf-16 and suppression of daf-2 and akt-1 expression. In immunocompromised mice, 20% HSP alleviated CTX-induced immune dysfunction by increasing peripheral white blood cells and lymphocytes, attenuating thymic atrophy, and reducing hepatic oxidative stress via MDA inhibition. Gut microbiota analysis revealed that 20% HSP restored microbial balance by suppressing Escherichia-Shigella and enriching beneficial genera, like Psychrobacter. These findings highlight 20% HSP and SPI’s conserved anti-aging mechanisms via daf-16 activation in C. elegans and immune–gut modulation in mice, positioning them as plant-derived nutraceuticals targeting oxidative stress and immune dysregulation. Full article

Background/Objectives: Traumatic brain injury (TBI) is a global leading cause of disability and death, with millions of new cases added each year. Oxidative stress significantly exacerbates primary TBI, leading to increased levels of intracerebral cell death, tissue loss, and long-term functional deficits in surviving patients. Catalase and superoxide dismutase (SOD) mitigate oxidative stress and play a critical role in dampening injury severity. This study examines the neuroprotective effects of the novel antioxidant alpha lipoic acid-based therapeutic, CMX-2043, on antioxidant enzymes in a preclinical TBI model via various drug administration routes. Methods: Piglets (n = 28) underwent cortical controlled impact to induce moderate–severe TBI and were assigned to placebo (n = 10), subcutaneous CMX-2043 (SQ, 10 mg/kg; n = 9), or intravenous CMX-2043 (IV, 9 mg/kg; n = 9) treatment groups. Treatments began 1 h after TBI induction and continued for 5 days. MRI was performed throughout the study period to evaluate brain recovery. Blood was collected at 1, 7, and 42 days post-TBI, and liver and brain tissues were collected at 42 days post-TBI to measure catalase and SOD activity. Results: CMX-2043 IV-treated piglets showed 46.3% higher hepatic catalase activity than placebo (p = 0.0038), while the SQ group did not show significant changes in hepatic catalase activity compared to placebo. In the brain, SQ-treated piglets had significantly higher catalase activity than both IV (p = 0.0163) and placebo (p = 0.0003) groups (45.8340 ± 3.0855, 36.4822 ± 1.5558, 31.6524 ± 1.3129 nmol/min/mg protein for SQ, IV, and placebo, respectively), while IV-treated piglets did not show significant changes compared to placebo. IV-treated piglets did exhibit 39.3% higher brain SOD activity than placebo (p = 0.0148), while the SQ group did not show a significant change. CMX-2043 treatment did not alter plasma antioxidant enzyme activity during the study period. Importantly, within CMX-2043 treated TBI groups, piglets with significantly decreased lesion volumes, midline shift, and combined swelling and atrophy had better brain recovery, determined by MRI on day 1, 7, and 42 days post-injury TBI, exhibited higher brain catalase activity at 42 days post-injury TBI regardless of administration route, suggesting a link between improved recovery and sustained local catalase activity. Conclusions: This study highlights the impact of administration route on tissue-specific antioxidant responses, with IV administration enhancing liver catalase and brain SOD activity, while SQ administration primarily elevated brain catalase activity. In addition, this study shows an association between increased brain catalase activity and decreased TBI brain lesioning, midline shift, and combined swelling and atrophy, thus emphasizing the role of antioxidant defenses in neuroprotection post-injury. Full article

To investigate the effects of feeding frequency on the growth, intestinal health, and metabolism of larval red-tailed catfish (Hemibagrus wyckioides) cultured in land-based circular tanks, a 56-day feeding trial was conducted. A total of 450 fish (8.47 ± 0.36 g) were randomly allocated to three feeding frequencies: twice (F2), three times (F3), and four times (F4) daily. The results revealed that the F3 group had a significantly better feed conversion rate, specific growth rate, and weight gain rate compared to the F4 group (p < 0.05). Lipase activity and villus height were also significantly greater in the F3 group compared to the other groups (p < 0.05). The transcriptome of the F3 group showed significant enrichment in immune- and metabolism-related pathways. Additionally, the F3 group had a higher abundance of beneficial Clostridium compared to the other groups. Plesiomonas was identified as the main contributor in the F3 group, and its abundance was significantly decreased in the F4 group (p < 0.05). These findings indicated that a feeding frequency of three times per day improves the growth performance of H. wyckioides in aquaculture by increasing the abundance of beneficial Clostridium and Plesiomonas, activating multiple immune pathways, and enhancing amino acid metabolism. Full article

The antioxidant capacity and modulation of oxidative stress by industrially processed açaí pulp extract from the Amazon (APEA) and its major anthocyanins, cyanidin 3-glucoside (C3G) and cyanidin-3-O-rutinoside (C3R), were evaluated as potential strategies for preventing cardiovascular diseases. The APEA was chemically characterized using ultrafast liquid chromatography-mass spectrometry (UFLC-MS), which revealed six main phenolic compounds. Notably, 9-(2,3-dihydroxypropoxy)-9-oxononanoic acid, acanthoside B, roseoside, cinchonine, and nonanedioate were identified for the first time in açaí extracts. In vitro antioxidant assays demonstrated that APEA exhibited strong DPPH- and ABTS-radical-scavenging activities (up to 80% inhibition and 65 mmol TE/100g DW, respectively) and showed ferrous- and copper-ion-chelating activities comparable to those of EDTA-Na₂ at higher concentrations (up to 95% inhibition). Hydroxyl and superoxide radical scavenging activities reached 80% inhibition, similar to that of ascorbic acid. In H₂O₂-treated H9c2 cardiomyocytes, APEA significantly reduced the intracellular ROS levels by 46.9%, comparable to the effect of N-acetylcysteine. APEA also attenuated menadione-induced oxidative stress in H9c2 cells, as shown by a significant reduction in CellROX fluorescence (p < 0.05). In vivo, APEA (100 mg/kg) significantly reduced CCl-induced hepatic lipid peroxidation (MDA levels), restored glutathione (GSH), and increased the antioxidant enzymes CAT, GPx, and SOD, demonstrating superior effects to C3G and C3R, especially after 21 days of treatment (p < 0.001). These findings suggest that Amazonian açaí pulp (APEA) retains potent antioxidant activity after industrial processing, with protective effects against oxidative damage in cardiomyocytes and hepatic tissue, highlighting its potential as a functional food ingredient with cardioprotective and hepatoprotective properties. Full article