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Nanosized lanthanum oxide particles (La2O3) are commonly utilized in various industries. The potential health risks associated with La2O3 nanoparticles, cytotoxic effects at varying doses and time intervals, and the mechanisms behind their induction of behavioral changes remain uncertain and necessitate further investigation. Therefore, this study examined in vivo hepatotoxicity, considering the quantity (60, 150, and 300 mg/kg) and time-dependent induction of reactive oxygen species (ROS) over one week or 21 days. The mice received intraperitoneal injections of three different concentrations in Milli-Q water. Throughout the experiments, no physical changes or weight loss were observed among the groups. However, after 21 days, only the highest concentration showed signs of anxiety in the activity cage (p < 0.05). Subsequently, all animals treated with La2O3 NPs exhibited a significant loss of learning and memory recall using the Active Avoidances test, after 21 days (p < 0.001). Markers for anti-reactive oxygen species (ROS) such as superoxide dismutase (SOD) were significantly upregulated in response to all concentrations of NPs after seven days compared to the control group. This was confirmed by a significant increase in glutathione peroxidase (Gpx1) and pro-apoptotic Caspase-3 expression at the lowest and highest doses. Additionally, both transcription and protein levels of the anti-apoptotic BCL-2 surpassed P53 protein in a dosage-dependent manner, indicating activation of the primary anti-apoptosis pathway. After 21 days, P53 levels exceeded BCL-2 protein levels, confirming a significant loss of BCL-2 mRNA, particularly at the 300 mg/kg concentration. Furthermore, a higher transcription level of Caspase-3, SOD, and Gpx1 was observed, with the highest values detected at the 300 mg/kg concentration, indicating the activation of cell death. Histopathological analysis of the liver illustrated apoptotic bodies resulting from La2O3 NP concentration. The investigation revealed multiple inflammatory foci, cytoplasmic degeneration, steatosis, and DNA fragmentation consistent with increased damage over time due to higher concentrations. Blood samples were also analyzed to determine liver enzymatic changes, including alkaline phosphatase (ALP), alanine transaminase (ALT), aspartate aminotransferase (AST), and lipid profiles. The results showed significant differences among all La2O3 NP concentrations, with the most pronounced damage observed at the 300 mg/kg dose even after 21 days. Based on an animal model, this study suggests that La2O3 hepatotoxicity is likely caused by the size and shape of nanoparticles (NPs), following a dose and time-dependent mechanism that induces the production of reactive oxygen species and behavioral changes such as anxiety and memory loss., (© 2024. The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature.)

Lead is one of the cursed substances that threaten all human life. Lead poisoning can occur through food or water contaminations and it is hard to be detected. This incognito metal accumulates over time and resides in the liver, kidneys, and brain tissues leading to serious medical conditions, affecting organ functions, causing failure, kidney tubule degeneration, and destroying neuronal development. However, known metal chelators have bad negative effects. Asparagus officinalis (AO) is a promising herb; its root extract exhibited antioxidant, antiapoptotic, protective, and immunomodulatory activities. Inspired by those reasons, this study investigated to which extent Asparagus extract affected male mice's renal toxicity caused by lead acetate (LA) and antioxidant defense system. This work screened for its nephroprotective activity in four mouse groups: negative and positive control, LA group with renal injury, and diseased but pretreated mice with AO extract (AOE). Kidney index and kidney function biomarkers were evaluated. Antioxidant activities, lipid peroxidation, superoxide dismutase (SOD), catalase (CAT), glutathione reductase (GR), glutathione peroxidase (GPx), nitric oxide (NO), and reduced glutathione (GSH) were also tested. Furthermore, inflammatory cytokine (tumor necrosis factor-α (TNF-α), interleukin-1 β (IL-1β), and the nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB)), inducible nitric oxide synthase (iNOS), renal pro-apoptotic protein (Bax), antiapoptotic protein (Bcl-2), and caspase-3 levels were evaluated. The results showed that LA administration induced oxidative stress, renal inflammation, apoptosis, and renal histopathological alteration. However, due to its antioxidant activities, AOE was found to restrain oxidative stress, therefore preventing inflammation and apoptosis. Collectively, AOE perfectly clogged lead poisoning sneaking, stopped the bad deterioration, and succeeded to protect kidney tissues from toxicity, inflammation, and apoptosis., (© 2023. The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature.)

Poisoning by arsenic affects people worldwide, and many human illnesses and health issues, including neurotoxicity, have been linked to chronic exposure to arsenic. When exposed to arsenic, the body produces intracellular reactive oxygen species (ROS), which influence a variety of alterations in cellular activity and directly harm molecules through oxidation. Arsenic-induced lesions are improved by antioxidants with the ability to lower ROS levels. Therefore, the current research aimed to assess how well apigenin protected PC12 cells from the toxicity caused by inorganic arsenic salt (iAs). For 24 and 48 h, iAs and/or apigenin were applied to PC12 cells. Then, oxidative stress indicators like malondialdehyde (MDA), nitric oxide (NO), and ROS in addition to the enzymatic and non-enzymatic antioxidant molecules such as catalase (CAT), glutathione (GSH), and superoxide dismutase (SOD) were assessed. Moreover, after exposure to iAs, PC12 was examined for nuclear factor erythroid 2-related factor 2 (Nrf2) expression to clarify how apigenin manifests its neuroprotection. Furthermore, NF-kB p65 concentration and IL-1B, IL-6, and TNF-α mRNA expression were measured to assess neuroinflammation. Bax, caspase-3, and Bcl-2 levels were measured to investigate apigenin's potential to protect PC12 cells from iAs poisoning. The obtained results revealed that, the cell survival rate in the iAs group was significantly lower (P < 0.05), and the number of viable cells steadily increased after apigenin treatment. Furthermore, the study found that iAs decreased GSH, CAT, and SOD in the PC12 cells while increasing ROS, MDA, and NO levels. In PC12 cells, the capacity of iAs to cause oxidative stress was linked to the induction of neuroinflammation and apoptosis. Interestingly, apigenin pre-treatment of PC12 cells resulted in exceptional protection against iAs-induced neuroinflammation, oxidative stress, and apoptotic cell death. Nrf2 upregulation in PC12 cells may explain the neuroprotection effect of apigenin against iAs toxicity. In conclusion, the obtained results of the present study have clinical significance and indicate that apigenin is a promising candidate for shielding the nervous system from toxic effects caused by arsenic. These findings require further investigation using in vivo experimental models., (© 2023. The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature.)

One of the most prevalent harmful heavy metals is lead (Pb). It is generally recognized to be harmful to the testicles. Asparagus officinalis has many saponins, flavonoids, and other phenolics with strong antioxidant and anti-inflammatory effects. The effects of A. officinalis (asparagus) aqueous extract (AOAE) on testicular damage caused by lead acetate (PbAc) were investigated in this study. In this way, 20 mg/kg PbAc was injected intraperitoneally 2 h after mice were administered 400 mg/kg AOAE orally for 14 days. In the biochemical analysis of testicular tissue, PbAc decreased enzymatic and nonenzymatic antioxidant molecules in testicular tissue, while increasing lipid peroxidation, nitric oxide, inflammatory markers [nuclear factor kappa-B (NF-κB), tumor necrosis factor-alpha (TNF-α), interleukin-1beta (IL-1 β), IL-6, and inducible nitric oxide synthase (iNOS)], and apoptotic-related proteins. Additionally, PbAc was discovered to reduce sperm motility and increase the percentage of dead sperm. However, due to its antioxidant qualities, AOAE has been found to reduce oxidative stress, therefore protecting against inflammation and apoptosis. It also allowed the AOAE sperm parameters to restore to their previous values in the control group. According to the findings, AOAE could be a natural substance that could be used to treat Pb-induced testicular toxicity; this protection may be attributed to its anti-oxidative, anti-inflammatory, and anti-apoptotic effects. However, this study warrants further works to explore in detail the underlying mechanisms of the alleviating effects of AOAE against Pb-induced toxicity and which of its active ingredients is responsible for this protection., (© 2022. This is a U.S. Government work and not under copyright protection in the US; foreign copyright protection may apply.)

The utilization of novel compounds as cancer treatments offers enormous potential in this field. The advantages of nanomedicine-based therapy include efficient cellular uptake and selective cell targeting. In this study, we employ selenium nanoparticles' green-synthesized by apigenin (SeNPs-apigenin) to treat breast cancer. We used various assays to show that SeNPs-apigenin can reduce MCF-7 cell viability and trigger apoptosis in vitro. Flow cytometry and PCR methods were used to detect apoptosis, while cell migration and invasion methods were used to quantify the possible effect of SeNPs-apigenin therapy on cell migration and invasion. According to cytotoxicity testing, the SeNPs-apigenin treatment can successfully limit MCF-7 cell proliferation and viability in a concentration-dependent manner. Flow cytometric and PCR analyses revealed that SeNPs-apigenin treatment induced apoptosis in MCF-7 cells, demonstrating that SeNPs-apigenin treatment could directly target Bcl-2, Bax, and caspase-3 and result in the discharge of cytochrome C from mitochondria into the cytosol, accompanied by the initiation of cell death, leading to permanent DNA damage and killing of MCF-7 cells. Furthermore, treatment with SeNPs-apigenin increased reactive oxygen species production and oxidative stress in MCF-7 cells. Our findings indicate that SeNPs-apigenin has cytotoxic potential in the treatment of breast cancer., (© 2022. The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature.)

Coronavirus disease 2019 (COVID-19) is a rapidly growing pandemic that requires urgent therapeutic intervention. Finding potential anti COVID-19 drugs aside from approved vaccines is progressively going on. The chemically diverse natural products represent valuable sources for drug leads. In this study, we aimed to find out safe and effective COVID-19 protease inhibitors from a library of natural products which share the main nucleus/skeleton of FDA-approved drugs that were employed in COVID-19 treatment guidelines or repurposed by previous studies. Our library was subjected to virtual screening against SARS-CoV Main protease (Mpro) using Molecular Operating Environment (MOE) software. Twenty-two out of those natural candidates showed higher binding scores compared to their analogues. We repurpose these natural products including alkaloids, glucosinolates, and phenolics as potential platforms for the development of anti-SARS-CoV-2 therapeutics. This study paves the way towards discovering a lead used in the treatment of COVID-19 from natural sources and introduces phytomedicines with dual therapeutic effects against COVID-19 besides their original pharmacological effects. We recommend further in vitro evaluation of their anti-COVID-19 activity and future clinical studies., (© 2021. The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature.)

Coronavirus disease (COVID-19) is an emerging pandemic that threatens the world since the early days of 2020. Development of vaccines or new drugs against COVID-19 comprises several stages of investigation including efficacy, safety, and approval studies. A shortcut to this delicate pathway is computational-based analysis of FDA-approved drugs against assigned molecular targets of the coronavirus. In this study, we virtually screened a library of FDA-approved drugs prescribed for different therapeutic purposes against versatile COVID-19 specific proteins which are crucial for the virus life cycle. Three antibiotics in our screening polymyxin B, bafilomycin A, and rifampicin show motivating binding stability with more than one target of the virus. Another category of tested drugs is oral antiseptics of mouth rinsing solutions that unexpectedly exhibited significant affinity to the target proteins employed by the virus for attachment and cell internalization. Other OTC drugs widely used and tested in our study are heartburn drugs and they show no significant binding. We tested also some other drugs falling under the scope of investigation regarding interference with a degree of severity of COVID-19 like angiotensin II blockers used as antihypertensive, and our study suggests a therapeutic rather than predisposing effect of these drugs against COVID-19., (© 2021. The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature.)

In more than two-thirds of the diabetic foot ulcer (DFUs) cases, lower limb amputation of foot ulceration is caused by the infection. The role of transition a metal complex as a therapeutic compound is becoming increasingly important. In vitro, four groups of antibiotics and one sulfa drug were tested against diabetic foot resistant bacteria. Using three concentrations of two different prepared metal complexes: copper (Cu) and silver (Ag) - isoniazid (Iso) and nicotinamide (Nicot) were tested against diabetic foot isolates. Results revealed that β-lactam drugs (cephradine and piperacillin) showed the minimum averages of MIC 265 μg/ml against Gram-positive and Gram-negative isolates. Silver isoniazid (Iso-Ag-1) metal complex was selected depending on the maximum averages of MIC against both types of clinical isolates. The combination between β-lactams and Iso-Ag-1 showed maximum FICI averages of 0.24 for Gram-positive and 0.28 for Gram-negative. In addition, a combination between Iso-Ag-1 with squilla chitosan nanoparticles (CSSq-nAg) showed averages of synergistic index by 0.23 against Staphylococcus aureus and 0.13, 0.30, and 0.27 against E. coli, K. pneumoniae, and Ps. aeruginosa, respectively. Final formula of Iso-Ag-1+CSSq-nAg + β-lactams (cephradine and piperacillin) showed a synergistic effect at FICI = 0.044 and 0.047, against G+ve and -ve, respectively. These two combinations showed a slight toxicity against the water flea Daphnia magna by 3.49 and 3.6 ppm, respectively. Results suggest the use of Iso-Ag-1-CSSq-nAg as enhancing agent in combination with β-lactams as a blind therapy in pharmaceutical preparations., (© 2021. The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature.)

The World Health Organization (WHO) recognized a novel coronavirus as the causative agent of a new form of pneumonia. It was subsequently named COVID-19 and reported as the source of a respiratory disease occurrence starting in December 2019 in Wuhan, Hubei Province, China. It has been affirmed a public health emergency of international significance by the World Health Organization. It is regarded as a subset of the severe acute respiratory syndrome (SARS) and the Middle East respiratory syndrome (MERS); COVID-19 is triggered by a betacoronavirus called SARS-CoV-2, which affects the lower respiratory tract and occurs in humans as pneumonia. A variety of drugs, such as remdesivir and favipiravir, are currently undergoing clinical trials to evaluate for the management of COVID-19. The effect of the pandemic as well as the epidemic that follows through the life cycles of various recycled plastic is evaluated, particularly those required for personal safety and health care. In response to the growth in COVID-19 cases worldwide, the energy and environmental impacts of these lifecycle management have risen rapidly. However, significant hazardous waste management concerns arise due to the need to assure the elimination of residual pathogens in household and medical wastes. This review article summarizes the preventive and environmental management of COVID-19., (© 2020. Springer-Verlag GmbH Germany, part of Springer Nature.)

Chlorpyrifos (CPF) is an extensive environmental contaminant and disrupts the physiological status of living organisms. CPF is found to hinder the health of aquatic organisms and ecological function in aquatic systems. The current study aimed at evaluating the protective effects of vitamin C (VC) on the immune response, hematological parameters, and histopathological alterations in Nile tilapia exposed to CPF. Nile tilapia were exposed to waterborne CPF (15 μg/L) for 30 days. Fish were divided into control group: received basal diet; CPF group: received basal diet and exposed to waterborne CPF; VC group: received basal diet plus 0.8 mg VC/kg; and CPF/VC group: received basal diet plus 0.8 mg VC/kg and exposed to waterborne CPF. Blood samples were taken after 15 days and 30 days of the treatment. Liver, gills, and intestine tissues were collected on the 30th day of treatment. CPF showed a deleterious effect on fish's growth performance; it decreased the weight gain by 6%, while VC increased it by 17-23% compared to the control group. CPF group recorded the lowest survival rate (83%), while VC achieved survivability of 96.7% and 93.3% in VC and CPF/VC groups, respectively. The blood picture revealed moderate changes in the CPF group, where the marked alteration was in the hemoglobin concentration and white blood cells. CPF disrupted the hepatic and renal function. Serum lysozyme activity, phagocytic activity, and phagocytic index displayed a dramatic decline in the CPF group but enhanced in VC and CPF/VC groups. An upregulation was observed in antioxidant genes (catalase and glutathione peroxidase), heat shock protein 70, caspase-3, and the cytokines interleukin 1β, interleukin 8, and interferon-gamma in the CPF group. Simultaneously, moderate or normal levels were shown in the VC and CPF/VC groups. CPF altered the histoarchitecture of gills, intestine, and hepatopancreas with apparent degenerative changes possibly resulted from the oxidative stress. At the same time, VC retained the normal structure of the studied tissues. This study raises concerns about the safety of CPF and its impact on the aquatic environment. VC has a high potential to restore the normal physiology of fish exposed to CPF.

Metal nanomaterials such as bismuth oxide nanoparticles (Bi 2 O 3 NPs) have been extensively used in cosmetics, dental materials, pulp capping, and biomedical imaging. There is little knowledge about the health risk of Bi 2 O 3 NPs in humans, which warrants a thorough toxicity investigation of Bi 2 O 3 NPs at the cellular level. In this experiment, we investigated the cytotoxic effect of Bi 2 O 3 NPs on human breast cancer (MCF-7) cells over 24 and 48 h. MCF-7 cells were exposed to Bi 2 O 3 NPs at varying doses (0.1, 0.5, 1.0, 5, 10, 20, 40 μg/mL) for 24 and 48 h. We assessed the toxicity of Bi 2 O 3 NPs by measuring its effect on the viability and oxidative stress biomarkers, e.g., GSH, SOD, and catalase in MCF-7 cells. The pro-apoptotic effects of Bi 2 O 3 NPs on MCF-7 cells were determined via evaluating dysfunction of mitochondrial membrane potential (MMP), caspase-3 activity, externalization of phosphatidylserine, and chromosome condensation. Furthermore, apoptotic cells were evaluated using 7-AAD fluorescence stain and Annexin V-FITC. Bi 2 O 3 NPs induced oxidative stress in MCF-7 cells in a time- and dose-dependent manner. Bi 2 O 3 NPs increased the rate of both necrotic cells and apoptotic cells. In addition, the blue fluorescence of MCF-7 cells with condensed chromatin was increased in a time- and dose-dependent manner. In conclusion, the present study highlights the potential toxic effects of Bi 2 O 3 NPs at the cellular level and suggests further investigation of Bi 2 O 3 NPs before any medical purposes.

Diabetes mellitus (DM) is one of the most dangerous incurable diseases that affects a large number of people worldwide. Artemisia species have various protective activities and are widely used for the control of diabetes in folkloric medicine. Therefore, the current study was designed to illustrate the protective effect of oral administration of Artemisia judaica extract (AjE) against hepatorenal damage in a high-fat diet/streptozotocin (HFD/STZ) rat model of hyperlipidemia and hyperglycemia. Animals were divided into five groups-control, AjE, HFD/STZ, HFD/STZ-AjE (300 mg/kg), and HFD/STZ-MET (100 mg/kg)-and treated daily for 28 days. The results revealed that STZ-injected rats showed marked hyperglycemia and hypoinsulinemia in addition to high levels of cholesterol, triglycerides, and low- and high-density lipoproteins compared to control rats. Significant elevations in hepatic (AST and ALT) and renal (urea, uric acid, and creatinine) function markers were observed in the serum of diabetic rats. Additionally, STZ injection caused remarkable elevations in lipid peroxidation and nitric oxide levels as well as suppression of antioxidant markers (superoxide dismutase, catalase, glutathione peroxidase, glutathione reductase, and glutathione). Marked elevations in TNF-α and Bax levels with a decline in Bcl-2 levels were detected after STZ injection. Furthermore, TGF-β1 expression levels were significantly upregulated in the liver and kidney tissues. Rats that received AjE or MET showed significant improvement in most of the aforementioned parameters, and the protective efficacy was higher for AjE than for MET. Histopathological screening confirmed the biochemical findings. Conclusively, our results illustrated the antihyperglycemic, antihyperlipidemic, antioxidant, anti-inflammatory, and antiapoptotic activities of AjE against hepatorenal injury in HFD/STZ-induced diabetes.

Lead (Pb) is an environmental toxicant; its consumption can induce renal deficits. In this study, we explored the possible protective efficiency of Moringa oleifera extract (MOE) against lead acetate (PbAc)-mediated reprotoxicity. Four experimental groups of seven rats each were used: control, PbAc, MOE, and MOE+PbAc groups. All groups were given their respective treatment for 4 weeks. PbAc impaired the oxidative/antioxidative balance in the renal tissue, as shown by the decreased antioxidant proteins (glutathione, glutathione reductase, glutathione peroxidase, catalase, and superoxide dismutase) and increased oxidants (lipid peroxidation and nitric oxide). Additionally, PbAc enhanced the progression of kidney inflammation by increasing tumor necrosis factor-alpha, interleukin-1 beta, and nuclear factor kappa B associated with upregulation of inducible nitric oxide synthase. Moreover, a dysregulation in the apoptotic-regulating proteins (Bax, caspase-3, and Bcl2) were recorded upon PbAc exposure. Remarkably, MOE oral administration restored redox homeostasis, suppressed the inflammatory and apoptotic responses in the kidney tissue. Our findings point out that MOE could be used as an alternative remedy to overcome the adverse effects of Pb exposure, which may be due to its potent antioxidant, anti-inflammatory, and anti-apoptotic effects.

This experiment explored the potential hepatic protective effect of Moringa oleifera Lam. methanolic extract (MOE) against lead-induced hepatotoxicity. Thirty-two adult Wistar albino rats were allocated randomly equally into four groups, seven rats each. The control group received intraperitoneal (i.p.) injections of physiological saline (0.9% NaCl); the lead acetate (Pb) group was i.p. injected with 20 mg/kg of Pb; the MOE group was orally administered with 250 mg/kg of MOE; and the MOE+ Pb group was orally treated with 250 mg/kg of MOE 3 h before receiving i.p. injections of 20 mg/kg Pb. All rats received their treatment for 14 days. Results revealed that Pb(II) intoxication induced liver injury accompanied by elevated levels of liver function markers (ALT and AST), oxidative stress markers (MDA and NO), and proinflammatory cytokines (NF-κB p65, TNFα, and IL-1β as well iNOS expression) in addition to the pro-apoptotic-related proteins such as Bax and caspase-3. Meanwhile, significantly depleted GSH content, suppressed activity of antioxidant enzyme activity, and anti-apoptotic protein Bcl-2 were also manifested in the liver tissue. Interestingly, concurrent treatment of rats with MOE ameliorated liver markers, prevented tissue injury, and inhibited oxidative stress, apoptosis, and NF-κB. In addition, MOE activated the detoxifying enzyme system in Pb(II)-intoxicated rats. Therefore, the obtained results in the present experiment provide evidence that MOE concurrent administration has the potential to protect the liver tissues in Pb(II)-intoxicated rats by preventing oxidative stress, inflammation, and apoptosis, via attenuation of NF-κB signaling pathway.

Fipronil (FPN), a phenylpyrazole insecticide, has been receiving increased attention owing to its toxicity, which is largely mediated through its effects on antioxidant systems. The present study was undertaken to assess the effects of resveratrol (RSV) and curcumin (CUR) on oxidative damage induced by FPN. Forty mature male Wistar rats were randomized into five groups (n = 8 per group): the first group was the control; the second was administered FPN (10 mg/kg); and the third, fourth, and fifth were co-treated with RSV (10 mg/kg), CUR (200 mg/kg), and their combination, respectively, 2 h prior to FPN administration. All animals were dosed via oral gavage for 4 weeks. FPN significantly (p < 0.05) elevated the sera of alanine aminotransferase (ALT), aspartate aminotransferase (AST), alkaline phosphatase (ALP), lactate dehydrogenase (LDH), γ-glutamyl transferase (GGT), urea, creatinine, and cholesterol levels, whereas serum total protein, albumin, and triglyceride levels were significantly (p < 0.05) decreased, compared to those of the control group. Reduced glutathione (GSH), superoxide dismutase (SOD), glutathione peroxidase (GPx), and catalase (CAT) were decreased (p < 0.05) in the FPN-treated group compared to those in the control group; however, malondialdehyde (MDA) and nitric oxide (NO) levels were markedly increased (p < 0.05) in the hepatic, renal, and brain tissues. Co-treatment with RSV or CUR alleviated (p ˂ 0.05) the increased lipid peroxidation and changes in enzymatic/nonenzymatic antioxidants induced by FPN; all these variables mostly returned to normal levels with the combined of RSV and CUR treatment. In conclusion, RSV and/or CUR relieved and synergistically reversed the FPN-induced tissue oxidative injury, probably by improving the antioxidant defenses via their free radical scavenging and antioxidant characteristics.

Acrylamide (AA) is a heat-induced toxin formed during thermal processing of many commonly consumed foods, including meat products, French fries, potato crisps, bread, cereals, cookies, and coffee. There is thus potentially high dietary exposure of humans to AA, which can induce significant oxidative stress. Hesperidin (HS) and diosmin (DS) are flavone glycosides that have antioxidant properties. The aim of this study was to investigate the protective effects of HS and DS against AA toxicity. Fifty-six adult male Wistar albino rats were divided into seven groups. The first group was orally administered 0.5% (w/v) dimethyl sulfoxide (DMSO) and considered as the control group. The second and third groups were orally administered 10 mg/kg/day of HS or DS, respectively. The fourth group received 20 mg/kg/day of AA orally for 14 days. The fifth and sixth groups were given 10 mg/kg/day of HS or DS, respectively, followed by AA. The seventh group was given both HS and DS after AA administration. AA intoxication significantly (p ≤ 0.05) increased serum levels of liver function enzymes (ALT, AST, and ALP), kidney function products (urea and creatinine), oxidative DNA damage marker (OHdG), proinflammatory markers (TNF-α, IL-1β, and IL-6), lipid peroxidation marker (malondialdehyde), and nitric oxide (NO). On the other hand, it significantly (p ≤ 0.05) decreased levels of reduced glutathione (GSH) in the liver, kidney, and brain. The activities of glutathione peroxidase (GSH-Px), superoxide dismutase (SOD), and catalase (CAT) in the liver, kidney, and brain tissues were also reduced. HS and DS supplementation prevented lipid peroxidation, normalized the serum parameters altered by AA, and enhanced the tissue concentrations and activities of antioxidant biomarkers. It could be concluded that HS and DS have potent protective effects against oxidative stress, lipid peroxidation, and DNA damage induced by AA toxicity in rats.