Protective Role Of N-acetylcysteine Research Articles

The Possible Protective Role of N-acetylcysteine against Testicular Toxicity Induced by Paracetamol Overdose in Adult Male Rats

The Possible Protective Role of N-acetylcysteine against Testicular Toxicity Induced by Paracetamol Overdose in Adult Male Rats

Silver nanoparticles induce endothelial cytotoxicity through ROS-mediated mitochondria-lysosome damage and autophagy perturbation: The protective role of N-acetylcysteine

Silver nanoparticles (AgNPs) are used increasingly often in the biomedical field, but their potential deleterious effects on the cardiovascular system remain to be elucidated. The primary aim of this study was to evaluate the toxic effects, and the underlying mechanisms of these effects, of AgNPs on human umbilical vein endothelial cells (HUVECs), as well as the protective role of N-acetylcysteine (NAC) against cytotoxicity induced by AgNPs. In this study, we found that exposure to AgNPs affects the morphology and function of endothelial cells which manifests as decreased cell proliferation, migration, and angiogenesis ability. Mechanistically, AgNPs can induce excessive cellular production of reactive oxygen species (ROS), leading to damage to cellular sub-organs such as mitochondria and lysosomes. More importantly, our data suggest that AgNPs causes autophagy defect, inhibits mitophagy, and finally activates the mitochondria-mediated apoptosis signaling pathway and evokes cell death. Interestingly, treatment with ROS scavenger-NAC can effectively suppress AgNP-induced endothelial damage.Our results indicate that ROS-mediated mitochondria-lysosome injury and autophagy dysfunction are potential factors of endothelial toxicity induced by AgNPs. This study may provide new evidence for the cardiovascular toxicity of AgNPs and serve as a reference for the safe use of nanoparticles(NPs) in the future.

Protective role of N-acetylcysteine and Sulodexide on endothelial cells exposed on patients' serum after SARS-CoV-2 infection.

Severe acute respiratory syndrome coronavirus-2 causes hyperinflammation and activation of coagulation cascade and, as a result, aggravates endothelial cell dysfunction. N-acetylcysteine and Sulodexide have been found to mitigate endothelial damage. The influence on coronary artery endothelial cells of serum collected after 4 ± 1 months from coronavirus infection was studied. The concentrations of serum samples of interleukin 6, von Willebrand Factor, tissue Plasminogen Activator, and Plasminogen Activator Inhibitor-1 were studied. The cultures with serum of patients after coronavirus infection were incubated with N-acetylcysteine and Sulodexide to estimate their potential protective role. The blood inflammatory parameters were increased in the group of cultures incubated with serum from patients after coronavirus infection. Supplementation of the serum from patients after coronavirus infection with N-acetylcysteine or Sulodexide reduced the synthesis of interleukin 6 and von Willebrand Factor. No changes in the synthesis of tissue Plasminogen Activator were observed. N-acetylcysteine reduced the synthesis of Plasminogen Activator Inhibitor-1. N-acetylcysteine and Sulodexide increased the tPA/PAI-1 ratio. N-acetylcysteine may have a role in reducing the myocardial injury occurring in the post-COVID-19 syndrome. Sulodexide can also play a protective role in post-COVID-19 patients.

The possible protective role of N-acetyl cysteine against tamoxifen-induced hepatotoxicity in the adult female albino rats: Biochemical and Histological study

The possible protective role of N-acetyl cysteine against tamoxifen-induced hepatotoxicity in the adult female albino rats: Biochemical and Histological study

Protective effect of N-acetyl cysteine on the mitochondrial dynamic imbalance in temporal lobe epilepsy: Possible role of mTOR

Understanding the underlying molecular mechanisms involved in epilepsy is critical for the development of more effective therapies. It is believed that mTOR (Mechanistic Target of Rapamycin kinases) activity and the mitochondrial dynamic balance change during epilepsy. mTOR affects mitochondrial fission by stimulating the translation of mitochondrial fission process 1 (MTFP1). In This study, the protective role of N-acetylcysteine was studied in temporal lobe epilepsy (TLE) through the regulation of mTOR and mitochondrial dynamic proteins. Rats received N-acetylcysteine (oral administration) seven days before induction of epilepsy, followed by one day after epilepsy. TLE was induced by microinjection of kainite into the left lateral ventricle. The total mTOR and Drp1 levels in the hippocampus were evaluated by western blotting. MFN1 was assessed using immunohistochemistry, and the expression of Fis.1 and MTFP1 (fission-related proteins) and OPA (fusion-related protein) were detected by real-time PCR. The mitochondrial membrane potential was measured by Rhodamin 123. The results showed that 72 h after induction of epilepsy, the mTOR protein level increased, and the balance of the mitochondrial dynamic was disturbed; however, oral administration of NAC decreased the mTOR protein level and improved the mitochondrial dynamic. These findings indicate that NAC plays a neuroprotective role in temporal lobe epilepsy, probably through decreasing the mTOR protein level, which can improve the imbalance in the mitochondrial dynamic.

Anti-apoptotic properties of N-Acetyl cysteine and its effects on of Liver X receptor and Sirtuin 1 expression in the liver of rats exposed to Lead

BackgroundThis study aimed to evaluate the expression of Liver X receptor (Lxr), Sirtuin 1 (Sirt1), apoptotic-related genes, and the protective role of N-acetylcysteine (NAC) in the liver of rats treated with Lead (Pb). MethodsRats were randomly divided into 5 groups, including G1 (control), G2 (single dose of Pb), G3 (continuous dose of Pb), G4 (single dose of Pb + NAC), and G5 (continuous dose of Pb + NAC). Lipid profiles and liver specific enzymes were assessed. Expression of Lxr, Sirt1, Bax and Caspase-3 genes was considered using RT-PCR. ResultsExposure to Pb caused a significant accumulation of Pb in the blood and liver tissue, increase in serum AST, ALT and ALP enzymes, as well as lipid profiles. Chronic exposure to Pb caused a significant decrease in Lxr (3.15-fold; p < 0.001) and Sirt1 (2.78-fold; p = 0.009), but significant increase in expression of Bax (4.49-fold; p < 0.001) and Caspase-3 (4.10-fold; p < 0.001) genes when compared to the control. Combined therapy with Pb + NAC in rats caused a significant decrease in AST, ALT and ALP values (28.93%, 20.80% and 28.86%, respectively) in the blood as compared to rats treated with Pb alone. Co-treated with Pb + NAC significantly increased the expression of Lxr (1.72-fold; p = 0.043) and Sirt1 (2.45-fold; p = 0.008), but decreased the expression of Bax (1.96-fold; p = 0.03) and Caspase 3 (2.22-fold; p = 0.029) genes when compared to rats treated with Pb alone. ConclusionChronic exposure to Pb is strongly associated with accumulation of Pb in the blood and liver, hepatic cells apoptosis, down-expression of Lxr and Sirt1 genes and consequently liver injury and abnormal lipid profiles. NAC reversed the Pb-induced toxicity on the liver tissue.

Nephrotoxic effect of Hydrogen Cyanamide (Dormex) and possible protective role of N-acetyl cysteine in male albino rats

Nephrotoxic effect of Hydrogen Cyanamide (Dormex) and possible protective role of N-acetyl cysteine in male albino rats

The Possible Protective Role of N-acetylcysteine Against Gibberellic Acid-Induced Lung Structural Changes of the Adult Albino Rat

The Possible Protective Role of N-acetylcysteine Against Gibberellic Acid-Induced Lung Structural Changes of the Adult Albino Rat

The possible protective role of N-acetyl cysteine on duodenal mucosa of high fat diet and orlistat treated adult male albino rats and the active role of tumor necrosis factor α (TNFα) and Interleukin 6 (IL6) (histological and biochemical study)

ABSTRACT Background Obesity is a major universal health issue linked to a majority of illness. Aim To evaluate the histological and biochemical changes occurred in the duodenal mucosa of high fat diet HFD and orlistat fed rats and to assess the possible protective role of N-acetyl cysteine NAC supplementation. Material and method Sixty male albino rats weighing 180–200 g were classified randomly into control group I and three experimental groups (HFD group II, HFD + orlistat group III, and HFD + orlistat + NAC group IV). All experimental groups received HFD alone/and treatment for 6 weeks. Group III received orlistat (32 mg/kg/day) before meals and group IV received the same regimen as group III in addition to NAC (230 mg/kg/day) after meals. After completion of the experiment, duodenal sections were processed for histological examination, oxidative stress parameters, and semiqualitative real time PCR for proinflammatory mediators TNFα and IL6 evaluation. Also, plasma lipid parameters were assessed and morphometric duodenal results were analyzed statistically. Results By histological examination of HFD and (HFD + orlistat) groups, we found severe to moderate duodenal structural disturbances, increased goblet cells, collagen fibers, and BAX and iNOS immunostaining. By Biochemical examination, both groups showed increased proinflammatory markers level (TNFα and IL6) with decreased all antioxidant parameters and increased MDA. Moreover, NAC treatment in group IV significantly reduced all structural changes, levels of proinflammatory mediators and increased all antioxidant parameter levels and decreased MDA. Conclusion All findings elucidated that NAC could be accounted to be a useful drug for protection of duodenal mucosa of HFD and orlistat treated animals.

N-Acetyl cysteine mitigates histopathological changes and inflammatory genes expressions in the liver of cadmium exposed rats.

This study aimed to consider the expression of Nrf2, NLRP3 and caspase 1 genes, as well as oxidative stress, and the protective role of N-acetyl cysteine (NAC) in the liver of rats treated with cadmium (Cd). Male rats were randomly divided into five groups including G1 (control), G2 (single dose of Cd), G3 (continuous dose of Cd), G4 (single dose of Cd + NAC), and G5 (continuous dose of Cd + NAC). Levels of malondialdehyde (MDA) and total antioxidant capacity (TAC) were measured. Expression of Nrf2, NLRP3 and caspase 1 genes was considered using RT-PCR. NAC treatments significantly improved TAC, but decreased MDA values in rats that exposed to continuous dose of Cd (p<0.05). Exposure to continuous dose of Cd caused a significant decrease in Nrf2 expression by 2.46-fold (p<0.001), but enhanced expression of NLRP3 and Caspase 1 genes by 3.13-fold and 3.16-fold), respectively (p<0.001). Compared to rats that treated to continuous dose of Cd, NAC supplementation enhanced the expression of Nrf2 by 1.67-fold (p<0.001) and reduced the expression of NLRP3 and Caspase 1 genes by 1.39-fold (p<0.001) and 1.58-fold (p<0.001), respectively. Down-regulation of Nrf2 and overexpression of NLRP3 and caspase 1 seems to be one of the main mechanisms of Cd toxicity on liver tissue. NAC protects liver tissue against Cd-induced oxidative injuries via enhancement of Nrf2 expression and reduction of NLRP3 and caspase 1 genes.

L-Thyroxine induces left ventricular remodeling and fibrosis in rats by upregulating miR-21 in a reactive oxygen-dependent mechanism: a protective role of N-acetylcysteine

miR-21 is the most studied pro-fibrotic marker in the majority of mammalian tissues. The precise mechanism by which hyperthyroidism induces left ventricular LV fibrosis and remodeling remains unclear. In this study, we have investigated the role of miR-21 on l-thyroxine (l-Thy)-induced cardiac fibrosis in rats. Adult male Sprague–Dawley rats were divided into four groups as control, l-Thy, l-Thy + miR antagomir (inhibitor), and l-Thy + N-acetylcysteine (NAC/glutathione (GSH) precursor). Administration of l-Thy significantly increased mRNA levels of miR-21 in the LVs of the treated rats. Also, it impaired the LV systolic and diastolic function and increased the production of reactive oxygen species (ROS), the transactivation of NF-κB p65, the expression of NRLP3 inflammasome, and levels of tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) in these LVs. Concomitantly, l-Thy increased the ventricular collagen deposition, and stimulated the expression of collagen 1/3, alpha-smooth actin (α-SMA), transforming growth factor-β1, and Smad3/p-Smad3 but suppressed the expression of Smad7. All these effects were reversed by pre-treatment with miR-21 antagomir or co-administration of NAC. In conclusion, l-Thy-induced LV remodeling and fibrosis include a ROS-dependent upregulation of miR-21 which in turns activates NF-κB/NRLP3 inflammasome and suppresses SMad7.

NAC antagonizes arsenic-induced neurotoxicity through TMEM179 by inhibiting oxidative stress in Oli-neu cells

Arsenic is one of the most common environmental pollutants. Neurotoxicity induced by arsenic has become a major public health concern. However, the effects of arsenic-induced neurotoxicity in the brain and the underlying molecular mechanisms are not well understood. N-acetyl-cysteine (NAC) is a thiol-based antioxidant that can antagonize heavy metal-induced neurotoxicity by scavenging reactive oxygen species (ROS). Here, we used the mouse oligodendrocyte precursor cell (OPC) line Oli-neu to explore the neurotoxic effects of arsenic and the protective effects of NAC. We found that arsenic exposure decreased cell viability, increased oxidative stress, caused mitochondrial dysfunction, and led to apoptosis of Oli-neu cells. Furthermore, we revealed that NAC treatment reversed these neurotoxic effects of arsenic. TMEM179, a key membrane protein, was found highly expressed in OPCs and to be an important factor in maintaining mitochondrial functions. We found that TMEM179 played a critical role in mediating the neurotoxic effects of arsenic and the protective role of NAC. PKCβ is a downstream factor through which TMEM179 regulates the expression of apoptosis-related proteins. This study improves our understanding of the neurotoxic effects and mechanisms of arsenic exposure and the protective effects of NAC. It also identifies a potential molecular target, TMEM179, for the treatment of arsenic-induced neurotoxicity.

The effect of N-Acetyl cysteine on the expression of Fxr (Nr1h4), LXRα (Nr1h3) and Sirt1 genes, oxidative stress, and apoptosis in the liver of rats exposed to different doses of cadmium.

The aim of this study was to consider the expression of farnesoid X receptor (Fxr), liver X receptor (LXRα) and sirtuin 1 (Sirt1), oxidative stress, inflammation, apoptosis, and the protective role of N-acetylcysteine (NAC) in the liver of rats treated with cadmium (Cd). 30 Wistar rats were divided into 5 groups: G1 (control), G2 (single dose of Cd), G3 (continuous dose of Cd), G4 (single dose of Cd + continuous dose of NAC), and G5 (continuous dose of Cd + continuous dose of NAC). The apoptosis of hepatic cells was measured using the TUNEL assay. Levels of malondialdehyde (MDA), IL-10, TNF-α, and total antioxidant capacity (TAC) were measured by specific kits. The expression of Fxr, LXRα, and Sirt1 genes and ratio of Bax/Bcl2 was considered using RT-PCR. While NAC treatment improved TAC and IL-10 values, it decreased MDA and TNF-α levels in the liver of rats exposed to Cd (P < 0.001). NAC decreased Bax/Bcl2 in the liver of G4 and G5 groups (P < 0.001). Exposure to a continuous dose of Cd decreased Fxr, LXRα, and Sirt1 expression by 36.65- (P < 0.001), 12.52- (P < 0.001) and 11.34-fold (P < 0.001) compared to control, respectively. NAC increased Fxr, LXRα, and Sirt1 expression (P < 0.01) and decreased Cd concentrations in both serum and tissue samples in G4 and G5 groups. Our results suggested that NAC protects liver tissue against Cd toxicity by elevating antioxidant capacity, mitigating oxidative stress, inflammation, apoptosis and up-regulation of FXR, LXR, and SIRT1 genes.

Antioxidant, histopathological and biochemical outcomes of short-term exposure to acetamiprid in liver and brain of rat: The protective role of N-acetylcysteine and S-methylcysteine

The present study was conducted to investigate the protective effects of N-Acetyl-L-cysteine (NAC) and S-methyl- L-cysteine (SMC) against hepatic oxidative stress and brain damage induced by acetamiprid (ACP) in rats, which were evaluated by histopathological changes, measuring serum biomarkers and antioxidant defense systems. In this study, 42 rats were randomly divided into 6 groups and administered by intraperitoneally for one week: the control group, the sham group (normal saline), ACP alone (5 mg/kg) (group1), NAC alone (160 mg/kg) (group2), ACP + SMC (100 mg/kg) (group3), ACP + NAC (group 4) and ACP + NAC + SMC (group 5). Our results showed that acetamiprid induces liver injures including infiltration of inflammatory cells, congestion and altered histo-architecture and brain damages including gliosis, hyperemia and necrosis. The biochemical analyses showed that acetamiprid significantly altered the structural and biochemical profiles of liver which may be due to the loss of integrity of cell membranes. Furthermore, antioxidant parameters results of ACP group revealed that glutathione (GSH) and total antioxidant capacity (TAC) levels decreased significantly, while lipid peroxidation (LPO) content and glutathione-S-transferase (GST) and catalase (CAT) activities increased in both tissues (P < 0.05), suggesting tissue oxidative damage, which was also confirmed histopathological. Conversely, administration of NAC and SMC ameliorated LPO, GSH content and antioxidant enzymes system considerably (P < 0.05) in both tissues. Moreover, NAC and SMC administration also improved liver and brain malfunction. These results indicate that both NAC and in to a lesser amount SMC have a potent antioxidant protection in both tissues of rat against ACP-induced oxidative stress.

N‑acetylcysteine inhibits atherosclerosis by correcting glutathione‑dependent methylglyoxal elimination and dicarbonyl/oxidative stress in the aorta of diabetic mice.

In diabetic animal models, high plasma/tissue levels of methylglyoxal (MG) are implicated in atherosclerosis. N-acetylcysteine (NAC) is a cysteine prodrug that replenishes intracellular glutathione (GSH) levels, which can increase the elimination of MG in diabetes mellitus (DM). The present study investigated the anti-atherosclerotic role of NAC in DM and aimed to determine whether the mechanism involved GSH-dependent MG elimination in the aorta. Apolipoprotein-E knockdown (ApoE−/−) mice injected with streptozotocin for 5 days exhibited enhanced atherosclerotic plaque size in the aortic root; notably, a high-lipid diet aggravated this alteration. NAC treatment in the drinking water for 12 weeks decreased the size of the atherosclerotic lesion, which was associated with a reduction in MG-dicarbonyl stress and oxidative stress, as indicated by decreased serum malondialdehyde levels, and increased superoxide dismutase-1 and glutathione peroxidase-1 levels in the diabetic aorta. Endothelial damage was also corrected by NAC, as indicated by an increase in the expression levels of phosphorylated (p-)Akt and p-endothelial nitric oxide synthase (eNOS) in the aorta, as well as nitric oxide (NO) in the serum. In addition, MG-treated human umbilical vein endothelial cells (HUVECs) exhibited increased reactive oxygen species and decreased antioxidant enzyme expression levels. NAC treatment corrected the alteration in HUVECs induced by MG, whereas the protective role of NAC was blocked via inhibition of GSH. These findings indicated that the diabetic aorta was more susceptible to atherosclerotic lesions compared with non-diabetic ApoE−/− mice. Furthermore, NAC may offer protection against atherosclerotic development in DM by altering aortic and systemic responses via correcting GSH-dependent MG elimination, leading to decreased oxidative stress and restoration of the p-Akt/p-eNOS pathway in the aorta.

Testicular dysfunction in malathion induced toxicity in male rats: Protective role of NAC and Silymarin.

This study investigated the biochemical and histopathological testicular dysfunctions following subacute toxic exposure to malathion; and the potential counteracting effects of N-acetyl cysteine (NAC) and Silymarin against these induced toxic effects. The study was carried out on 48 Sprague-Dawley males, rats were divided into six equal groups, drugs were given by gastric gavage daily for 30 days as follow; control group: received distilled water, the group I: rats were treated with NAC at a dose 200 mg/kg/day; group II: rats were treated with Silymarin at a dose 200 mg/kg/day; group III: rats were given malathion at a dose of 200 mg/kg/day; group IV: rats were given malathion plus NAC; group V: rats were given malathion plus Silymarin. Significant reductions in the testicular weights were observed in malathion exposed rats. Malathion caused significant reductions in hormonal assay including follicle –stimulating hormone (FSH), luteinizing hormone (LH) and testosterone, butyryl cholinesterase activity as well, sperm counts and motility with significant increases in abnormal sperm morphology. The histopathological findings showed diffusely necrotic seminiferous tubules and arrested spermatogenesis. Administration of NAC and Silymarin improved the biochemical and histopathological alterations in the testes induced by malathion. However, NAC was much better than Silymarin for inducing these protective effects.

EFFECTIVENESS OF N-ACETYLCYSTEINE ON TITANIUM DIOXIDE NANOPARTICLES- INDUCED IMMUNOTOXICITY IN ADULT ALBINO RATS

Background: Titanium dioxide (TiO2) is a white pigment that can be used in paints, coatings, plastics, papers, inks, medicines, pharmaceuticals, food products, cosmetics, and toothpaste. Titanium dioxide nanoparticles (TiO2 NPs) have been reported to elicit various adverse cellular effects including oxidative stress and DNA damage. N-acetylcysteine (NAC) is an antioxidant and free radical scavenger used to combat oxidative stress-induced damage in various tissues. Aim of the Work: is to study the toxic effects of TiO2 NPs oral administration and the protective role of NAC on the immune system of adult male albino rats. Thirty adult male albino rats were divided into 4 groups: Group I subdivided into: Subgroup (A): negative control. Subgroup (B): positive control received 1 ml of 5% gum acacia solution by oral gavage once daily. Group II: gavaged orally 100 mg/kg NAC once daily. Group III:gavaged orally 1200 mg/kg titanium dioxide nanoparticles (1/10 LD 50) in 1ml of 5% gum acacia solution as a solvent once daily. Group IV: gavaged orally (100 mg/kg NAC then 1200 mg/kg TiO2 NPs once daily. After 6 weeks rats from each group and subgroup were subjected the following biochemical parameters: Tumor necrosis factor alpha and CBC with differential count. The rats were sacrificed and spleen was dissected and subjected to histopathological examination. Cell suspension from the spleen was examined to determine the extent of DNA damage through DNA extraction and gel electrophoresis. Conclusion: TiO2 NPs induced time dependent toxic effects and DNA damage in the spleen and administration of NAC with TiO2 NPs offers protection against their damaging effect. Recommendation: it is recommended to increase public awareness about health impact of TiO2 nanoparticles through nonessential drug additives, food colors, toothpastes etc.to limit their ingestion.

Protective Role of N-Acetylcysteine on the Cytotoxic Effect of Paclitaxel in MCF7 Breast Cancer Cell Line

N-Acetylcysteine (NAC) is a low molecular weight and thiol-containing antioxidant. The free radical scavenging property is linked to the nucleophilicity and redox interactions of the thiol group. The aim of this study was to investigate the cytotoxic effect of paclitaxel used in chemotherapeutic treatment of breast cancer and N-Acetylcysteine, an antioxidant molecule, on MCF7 cells. In the MCF7 breast cancer cell line, the cytotoxic effect of paclitaxel is 7.5 μM and 10 μM and N-acetylcysteine's 10mM, 25mM, 50mM, 75mM dose combinations on the cells were determined by WST1 test at 24, 48 and 72 hours incubation times. N-Acetylcysteine showed proliferative effect on breast cancer cells. This effect persisted when combined with paclitaxel and weakened the cytotoxic effect of paclitaxel. However, the proliferative effect of NAC decreased with increasing incubation time. Colony forming ability of applied combinations at MCF 7 cells is also supports the results of cytotoxicity. In vivo and in vitro longer-term studies that will be used concurrently with conventional cancer treatment and NAC will contribute to clarify the issue. Key words: N-Acetylcysteine, paclitaxel, MCF7 Special Issue of Health Sciences DOI: 10.7176/JSTR/6-03-23

Molecular mechanisms of Cisplatin- induced placental toxicity and teratogenicity in rats and the ameliorating role of N-acetyl-cysteine

The aim of the present study is to investigate the molecular mechanisms of Cisplatin- induced placental toxicity and teratogenicity in rats and the ameliorating role of N-acetyl-cysteine (NAC). Cisplatin was administrated intraperitoneally at 5 mg/kg.b.wt as a single dose on the 12th day of gestation while NAC was administered orally throughout gestation either alone or in concomitant injection of Cisplatin at 200 mg/kg.b.wt. Cisplatin + NAC group showed reduction in the elevated morphological, visceral and skeletal abnormalities as well as the morphological and histopathological changes in placenta compared to Cisplatin - treated rats. Importantly, NAC attenuated Cisplatin-induced placental apoptosis through down-regulation of Fas and Caspase-3 genes expression. In conclusion, induction of placental apoptosis by overexpression of Fas and Caspase-3 genes gives a new insight into the mechanism of Cisplatin teratogenicity. The protective role of NAC, on the other hand, was characterized by attenuation of Fas and Caspase-3 genes- mediated apoptosis.

The Possible Protective Role of N-Acetyl Cysteine against Titanium Dioxide Nanoparticles Intestinal Toxicity in Adult Male Albino Rats

Introduction: With extensive applications of nanoparticles including titanium dioxide nanoparticles (TiO2 NPs) in different fields, many adverse effects may threat both environmental and medical health. Aim of this work: To evaluate the role of n-acetyl cysteine (NAC) against TiO2 NPs intestinal toxicity in adult albino rats. Material and methods: Fifty adult male albino rats were classified into five groups. Group I: negative control received regular diet and water. Group II: positive control administered 1ml of 5% gum acacia solution once a day. Group III: gavaged orally with NAC (100 mg/kg). Group IV: orally gavaged with TiO2 NPs (1200 mg/kg) once a day. Group V: orally gavaged once daily with TiO2 NPs (1200 mg/kg) and NAC (100 mg/kg). After 6 weeks, all rats were weighed and blood sample were submitted to estimate serum level of citrulline. Then parts of ileum from all rats was dissected and subjected to interleukin 6 (IL6), interleukin 10 (IL10) and tumor necrosis factor (TNF-α) estimation, histopathological examination and determine the extent of DNA damage by gel electrophoresis. Results: The results revealed that TiO2 NPs induced significant decreases in body weight, and serum level of citrulline with significant increases in IL6, TNF-α and significant decrease IL10 in tissues of ileum. These were associated with histopathological changes in the ileum and DNA damage detected by gel electrophoresis. Co-administration of NAC with TiO2 NPs provided protection against these changes. Conclusion: TiO2 NPs exposure causes inflammation in ileum with DNA damage and administration of NAC offers protection against its damaging effects.