Toxicity In Adult Albino Rats Research Articles

Protective Effect of Aqueous Extract of Lawsonia Inermis (Henna) Leaves on Acetylsalicylic Acid Induced Gastric Mucosal Toxicity in Adult Albino Rats

Protective Effect of Aqueous Extract of Lawsonia Inermis (Henna) Leaves on Acetylsalicylic Acid Induced Gastric Mucosal Toxicity in Adult Albino Rats

Lambda-cyhalothrin-induced pancreatic toxicity in adult albino rats

Lambda-cyhalothrin (LCT) is one of the most frequently utilized pyrethroids. This study aimed to explore the toxic effects of subacute exposure to LCT on the pancreas and the hepatic glucose metabolism in adult male albino rats. 20 rats were equally grouped into; Control group and LCT group. The latter received LCT (61.2 mg/kg b.wt.), orally on a daily basis for 28 days. At the end of experiment, blood samples were collected for the determination of serum glucose and insulin levels. Pancreases were harvested and levels of malondialdehyde (MDA); catalase (CAT); superoxide dismutase (SOD); reduced glutathione (GSH); tumor necrosis factor-α (TNF-α); interleukin-6 (IL-6); nuclear factor erythroid 2–related factor 2 (Nrf2); heme oxygenase 1 (HO-1); and nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) were assessed. Also, liver samples were analyzed for the activity of glucose metabolism enzymes, glycogen content, and pyruvate and lactate concentrations. Histopathological and immunohistochemical examinations of pancreatic tissues were undertaken as well. Results revealed hyperglycemia, hypoinsulinemia, increased MDA, TNF-α, IL-6, and NF-κB levels, in association with reduced CAT, SOD, GSH, Nrf2, and HO-1 levels in LCT group. Liver analyses demonstrated a clear disturbance in the hepatic enzymes of glucose metabolism, diminished glycogen content, decreased pyruvate, and increased lactate concentrations. Besides, pancreatic islets displayed degenerative changes and β-cells loss. Immunohistochemistry revealed diminished area percentage (%) of insulin and Nrf2 and increased TNF-α immunoreaction. In conclusion, subacute exposure to LCT induces pancreatic toxicity, mostly via oxidative and inflammatory mechanisms, and dysregulates hepatic glucose metabolism in albino rats.

Possible Protective Effect of Grape Seed Extract and Curcumin on Triphenyltin Chloride Induced Thyroid Toxicity in Adult Albino Rats

Possible Protective Effect of Grape Seed Extract and Curcumin on Triphenyltin Chloride Induced Thyroid Toxicity in Adult Albino Rats

Curcumin ameliorated low dose-Bisphenol A induced gastric toxicity in adult albino rats

Bisphenol A (BPA) is one of the most common worldwide chemicals involved in the industry of polycarbonate plastics, medical devices, and pharmaceuticals. Forty three-month-old albino rats were randomly classified into four groups. Group Ӏ received a daily corn oil dose (5 mL/kg/ body weight, BW) through a gastric tube for one month, Group ӀӀ received a daily dose of Curcumin (200 mg/kg body weight (B.W.) through a gastric tube for one month, Group ӀӀӀ received a daily dose of BPA (0.5 μg/kg B.W.) through a gastric tube for one month and Group ӀV received concomitant daily doses of Bisphenol A and Curcumin as the regimen described in groups ӀӀ and ӀӀӀ. The rats were sacrificed, and glandular portion of stomach was dissected and processed for light, immunohistochemical and ultrastructural study. BPA induced destructed gastric glands, dilated congested blood vessels, submucosal oedema, decreased PAS-positive reactivity, increased collagen fibres deposition, decrease in the positive BCL2 immunoexpression, increased positive PCNA immunoexpression, reduction in the gastric mucosal height and destructive changes in the enteroendocrine, chief and parietal cells. Curcumin coadministration provoked an obvious improvement in the gastric structure. BPA exposure has toxic effects on the glandular portion of the stomach in rats. Otherwise, Curcumin coadministration has exhibited protective impact on the architecture of the stomach.

Hormonal Physiological Changes of Testis Resulting From Exposure to Vinyl Cyanide and the Possible Protective Role of β-cryptoxanthin in Male Rat

Vinyl cyanide (VCN) is an aliphatic nitrile product which is extensively used in various synthetic chemical industries. VCN is known to exert toxic actions to human beings as well as experimental animals. The present study was designed to examine the ability of β-cryptoxanthin, a naturally occurring antioxidant, to attenuate VCN-induced testicular toxicity in adult albino rats. Daily oral administration of VCN at a dose level of 30 mg/kg b.w. (7.2mg/ animal) to male rats for a period of 5 days significantly reduced the levels of serum testosterone (T), androsterone, follicle-stimulating hormone (FSH) and luteinizing hormone (LH) which indicates injury to the testis function. Compared to VCN-treated animals, pretreatment with β-cryptoxanthin and its co-administration with VCN once daily at a dose of 40 mg/kg b.w. (9.6mg/ animal) for 30 days induced a remarkable degree of improvement in the levels of endocrine parameters including T, androsterone, FSH and LH. In conclusion, the present results clearly demonstrate the protective role of β-cryptoxanthin against VCN-induced physiological changes in the testis of rats.

The possible protective effect of captopril on liver and bone marrow after cyclophosphamide-induced toxicity in adult albino rats

Cyclophosphamide (CP) is commonly used in regimen of treatment of cancers and autoimmune diseases as systemic lupus. Hepatotoxicity and bone marrow depression are acute side effects of CP through inducing oxidative stress. The concomitant use of captopril ameliorates these side effects. This study aimed to evaluate the possible protective effects of captopril against hepatotoxicity and bone marrow depression induced by CP in adult albino rats. In this experimental study, 60 rats were divided into 4 groups;, the captopril treated group (capoten tablet 50 mg/kg for 5 days orally), CP treated group (150 mg/kg, a single dose intraperitoneal administration) and the captopril-CP treated group received captopril (50mg/kg for 5 days orally) followed by CP (150 mg/kg, a single dose intraperitoneally). The liver tissues and bone marrow of rats in all groups were subjected to light and electron microscopic studies. The serum levels of liver function markers such as alanine aminotransferase (ALT) and aspartate aminotransferase (AST) were assessed in blood samples of each group as indicators of liver damage. The results showed that the injection of CP elevated serum ALT and AST compared to the control group. Concomitant treatment of captopril and CP decreases serum levels of ALT and AST. CP treated group showed diffuse lesion of liver tissue and bone marrow. The captopril-CP treated group showed minimal hepatic congestion and decreased adipose tissue in bone marrow. The current study provided that captopril has protective effect against cyclophosphamide induced hepatotoxicity and myelotoxicity.

Ameliorative effects of Green Tea Polyphenol Epigallocatechin-3-gallate on chlorpyrifos ovarian toxicity in adult albino rats

Chlorpyrifos (CPF) can induce ovarian damage and reproductive dysfunction through oxidative stress mechanisms. These can be reversed by antioxidants such as Epigallocatechin-3-gallate (EGCG) in green tea. This study aimed to investigate the toxicity effects of CPF on rat ovaries and the effectiveness of EGCG to protect against these effects. Fifty adult female albino rats were randomly assigned to five equal groups; negative and positive control groups, EGCG-treated group, CPF-treated group and CPF+EGCG-treated group. After four weeks the rat body weight and relative ovarian weight were estimated, and blood samples were collected to assess reproductive hormones (RHs) levels. Evaluation of ovarian oxidative stress indicators malondialdhyde (MDA), nitric oxide (NO), superoxide dismutase (SOD), reduced glutathione (GSH) and catalase (CAT) was performed. Ovarian sections were prepared and examined using the hematoxylin and eosin stain, proliferating cell nuclear antigen, and morphometric study to assess histopathologic changes. CPF-treated rats had significant lower body weight and relative ovarian weight compared to controls (P<0.001) and those treated with CPF+EGCG (P<0.001). CPF induced significant reduction in RHs levels and ovarian SOD, GSH and CAT activities when given alone, which were improved by the combined administration of CPF and EGCG. The levels of ovarian MDA and NO were significantly higher in CPF-treated rats than controls and rats treated with CPF+EGCG. The cellular proliferation in ovarian Graafian follicles was significantly suppressed in CPF-treated animals. Hence CPF can induce oxidative damage in rat ovaries, EGCG, a natural potent antioxidant, can be useful against the CPF toxicity effects in ovaries.

Can rutin ameliorate aluminum phosphide-induced acute cardiac toxicity in adult albino rats?

Current management of rice tablet or aluminium phosphide (AlP) poisoning has remained mostly supportive despite of its fatal outcome and unfortunately no antidote is found yet, therefore, there is a need to search for a treatment that can adequately protect against its toxicity. To the best of our knowledge, there are no studies until now concerning the cardioprotective effect of rutin against AlP cardiac toxicity in rats. For this purpose, this study was carried out to investigate the possible protective effect of rutin against AlP induced cardiotoxicity in rats. Forty male albino rats were randomly divided into four groups. Group I: normal control group was served as untreated rats and received distilled water orally through a gastric tube. Group II: Rutin treated group received a dose of 100 mg/kg rutin dissolved in distilled water and given orally through a gastric tube. Group III: AlP intoxicated rats received AlP oral single sub-lethal dose (2 mg/Kg body weight) dissolved in distilled water and given through a gastric tube. Group IV: AlP intoxicated rats + Rutin treated one hour after receiving AlP in doses as mentioned above. After that we tested the following parameters: ECG changes including HR and ST-segment elevation, serum level of TNF-α, IL-6 and H-FABP (pg/ml), antioxidant and Oxidant parameters in cardiac tissue as GSH, SOD, and MDA, apoptotic factor caspase-3 and histopathological examination of cardiac tissue was also included. The results showed that treatment with rutin caused a significant decrease in heart rate and ST segment elevation, a significant decrease in activity of TNF-α and IL-6 and levels of H-FABP also a significant decrease in the activity of SOD with decreased levels of MDA and caspase-3 level and a significant increase in the level of GSH compared to (AlP) intoxicated group, also histopathological changes induced by AlP improved after treatment with rutin. It is concluded that AlP intoxication caused ECG, biochemical and histopathological changes which were potentially improved with rutin. Â

Does Omega-3 Ameliorate Olanzapine-Induced Testicular Toxicity in Adult Albino Rats? A Histo-morphometric Study

Introduction: Olanzapine is one of the most frequently used antipsychotics that had undesirable effects on male sexual function. Aim of the work: To explore possible protective effect of omega-3 on olanzapine - induced testicular toxicity. Material and methods: Forty adult albino rats were used and alienated into four equal groups: I (control), II (omega-3 treated), III (olanzapine treated) and IV (olanzapine +omega-3 treated).Group I received vehicles of olanzapine and omega-3 orally once daily. Group II received 400 mg/kg/day of omega-3 orally. Group III received oral olanzapine 0.5 mg/kg/day. Group IV received a combination of the same mentioned doses of both drugs. After 14 weeks, testicular specimens were taken and processed for light and transmission electron microscopic study. Results: Group III showed shrunken degenerated seminiferous tubules (ST) with corrugated basement membrane whose lumina were devoid of spermatozoa. Few degenerated spermatogonia, primary spermatocytes, elongated spermatids and many Sertoli cells (SCs) were seen. The tubules were separated with wide interstitial spaces and congested blood vessels. Ultrastructural results revealed spermatogonia with degenerated nucleus, loss of nuclear membranes and cell boundaries of primary spermatocytes. Elongated spermatids appeared abnormal in shape with defects in acrosomal cap. A high significant decrease in mean ST diameter, height of germinal epithelium while a high significant increase in SCs count and number of caspase-3 immunopositive cells were observed. Group IV showed improvement of the previously mentioned results. Conclusion: Omega-3 could protect against olanzapine induced testicular toxicity therefore; it can be used as an adjuvant therapy with antipsychotic drugs.

Histoprotective effects of Curcumin on Bisphenol- A induced testicular toxicity in adult albino rats.

Endocrine Disrupting chemicals including bisphenols have contaminated the environment significantly and is known to damage spermatogenesis via increase in oxidative stress. The anti-oxidant properties of naturally occurring substances like curcumin have been well established. Objectives: To evaluate the protective effects of curcumin against bisphenol-A induced testicular damage. Study Design: Experimental Study. Setting: Department of Anatomy, University of Health Sciences, Lahore. Period: From March 2015 to December 2015. Material &amp; Methods: Thirty six rats were divided into four groups A, B, C and D of 9 animals each. Group A (control) was given 5ml/kg/day of corn oil orally for 10 days. Group B (Bisphenol-A) was given 100mg/kg/day of Bisphenol-A dissolved in corn oil orally for 10 days. Group C (recovery) was given 100mg/kg/day of BPA dissolved in corn oil orally for 10 days and left untreated for 10 days. Group D (Curcumin + BPA) was given 100mg/kg/day of BPA and 100mg/kg/day of Curcumin, dissolved in corn oil orally for 10 days. Rats of group A, B and D were sacrificed on day 11 and those of group C on day 21. After weighing the euthanized rats, testes were removed, processed and tissue sections were stained with H&amp;E for Johnson scoring and with PAS stain for assessment of basement membrane integrity. Results: Bisphenol-A administration caused a significant decrease in weight of animals, a significantly low Johnson score of seminiferous tubules and high frequency of disrupted basement membranes of the tubules in Group B as compared to control. The weight gain of animals improved in the with-drawl group C while no self-recovery was observed in other parameters. Curcumin co-administration improved the body weight gain of animals, increased the Johnson scoring of tubules significantly and partially restored the basement membrane integrity in group D, comparable to the control group. Conclusion: The results of this study indicate that co-administration of a potent antioxidant curcumin causes a significant antagonism of the histo-toxicity of testis produced by Bisphenol-A in albino rats.

The possible protective effects of saccharum officinarum l. (sugar cane) juice co-supplementation on gentamicin induced acute renal toxicity in adult albino rats

Gentamicin (GM) is an effective and probably the most commonly used aminoglycosides antibiotic, however the risk of causing nephrotoxicity limits its use. In the present study, the possible protective effects of Saccharum officinarum L. (sugar cane juice) on gentamicin induced acute oxidative renal injury in experimental rats were investigated. Twenty adult albino rats were randomly allocated into four groups (5 rats in each) and treated once daily for a period of 7 days as follows; group A being the negative control and was injected intraperitoneal with normal saline, group B (sugar cane juice treated group) was given sugar cane juice orally at a dose of 15 ml/kg/day, group C (GM treated group) and group D (sugar cane juice + GM treated group) were the experimental groups and were injected intraperitoneal with (80 mg/kg/day GM) &amp; (sugar cane juice 15 ml/kg/day orally + 80 mg/kg/day GM intraperitoneal) respectively. By the end of the experiment, the biochemical kidney functions tests (urinary cystatin C and kidney injury molecule-1, blood urea and creatinine) were investigated. Also, oxidative stress parameters (malondialdehyde [MDA] level, superoxide dismutase [SOD] &amp; glutathione peroxidase [GPX] enzymatic activity) in renal tissue were evaluated. Histopathological examinations of kidney were done to assess the degree of renal protection induced by sugarcane juice, Gentamicin treated rats showed; marked significant rise in the biochemical kidney functions tests and lipid peroxidation (MDA) parameter in renal tissues, along with significant reduction in renal tissue antioxidant enzymatic activity of both SOD &amp; GPX. However, co-administration of sugar cane juice in group D leading to marked reduction in previous biochemical markers and MDA levels together with significant elevated renal SOD &amp;GPX enzymatic activity which nearly tend to return to normal values. The histopathological examination of groups A and B showed normal kidney structure which was deranged in group C (GM treated), whereas group D showed significant recovery in histological structures. Gentamicin induced acute renal injury and oxidative damage. Co-administration of sugar cane juice may reduce this damage by improving antioxidant defense and tissue integrity in experimental albino rats.  Â

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.

The protective effect of Nigella Sativa oil on Penconazole induced -renal toxicity in adult albino rats: Histological, Immunohistochemical and Biochemical study

High doses of penconazole causing nephrotoxicity and renal damage. Nigella sativa (black seed) is one of the native plants. It has anti-inflammatory, antidiabetic and anti-cancerous properties.Aim: This work aimed to evaluate the effect of Nigella sativa oil on Penconazole induced renal toxicity in a rat model.Material and Methods: Sixty male adult albino rats were used . They were divided into equal four groups. Group I (control): rats were received distilled water Group II (N. sativa): rats were given orally 0.2ml N. sativa oil /100 g b. wt. three days/week for four weeks.Group III(PEN –treated): the animals were received intraperitoneally 67 mg penconazole /kg b. wt. three days/week for four weeks. Group IV(PEN+ N.sativa): rats were given penconazole (67 mg/kg b.w) and N. sativa oil (0.2ml/100 g) simultaneously three days weekly for four weeks. At the end of the experiment, kidney tissues were prepared for biochemical, immunohistochemical, light and electron microscopic studies.Results: Histological examination of penconazole treated group revealed glomerular atrophy, widening of the subcapsular space and hypercellularity of the glomerular cells. Detachment of podocytes and disruption of their processes resulted in impairment of the blood renal barrier. Tubular degeneration and necrosis were confirmed by significant decrease in Bcl2 immune marker. An increase in activity of intercalated cells of cortical collecting tubules was an indication of metabolic acidosis. Renal fibrosis was confirmed by an significant increase in α SMA and collagen fibers. Biochemical study revealed an increase in MDA level, decrease in both superoxide dismutase (SOD) and catalase (CAT).These changes were reserved by concomitant administration of Nigella sativa oil.Conclusion: The antioxidant properties of Nigella sativa could be attributed in ameliorating penconazole-induced nephrotoxicity in rats.

The Protective Role of Curcumin and Melatonin in Amelioration of Cadmium- Induced Cardiac Toxicity in Adult Albino Rats

Cadmium (Cd), a common toxic environmental and occupational pollutant which cause many organ toxicities probably due to its ability to induce oxidative stress. Curcumin and melatonin have many beneficial effects. THE AIM of this study is to investigate the possible role of curcumin and melatonin in amelioration of cadmium-induced cardiac toxicity in rats. METHODS: This study was conducted on 140 adult male albino rats divided into 7 equal groups. Group I served as negative control. Group II received curcumin in an oral dose of 200mg/kg/day. Group III received melatonin in an oral dose of 10mg/kg/day .Group IV received cadmium chloride an oral dose of 5.2mg/kg/day for 15 days. By using the same doses and period Group V received cadmium chloride and curcumin, Group VI received cadmium chloride and melatonin, Group VII received cadmium chloride, curcumin and melatonin. At the end of the experiment, rats were sacrificed and samples were collected. Serum markers of myocardial damage were measured includingcreatine kinase –MB isoform (CK-MB) , lactate dehydrogenase (LDH) ,cardiac Troponin I (cTn-I). Oxidative status was evaluated by estimation of superoxide dismutase (SOD), catalase (CAT) and glutathione -S transferase (GST) activity Total antioxidant capacity (TAC) in serum in addition to tissue malondialdehyde (MDA) in heart. RESULTS: Compared to negative control group, there was insignificant difference in the mean values of all the tested parameters in groups II and III, while significant difference was found in group IV. Group V showed significant difference from cadmium chloride group regarding all studied parameters but in comparison with control group, there was insignificant difference regarding cardiac parameters only. On the other hand, Group VI showed significant difference from Cd chloride group regarding all studied parameters and in comparison with control group, there was insignificant difference regarding cardiac parameters and SOD. As for Group VII, it showed significant difference from Cd chloride group, and insignificant difference from control group regarding all studied parameters. CONCLUSION: Cadmium chloride caused significant oxidative cardiac toxicity. Co- administration of melatonin could improve such toxicity more significantly than curcumin did, while co-administration of both melatonin and curcumin provided superior protection against Cd chloride toxicities compared to either of them alone. RECOMMENDATIONS: Further research is needed to investigate the beneficial effects of curcumin and melatonin and its applicability in humans vulnerable to Cd toxicity.

Role of Ginseng on mercury chloride-induced testicular lesions in adult albino rat

Background Mercury is a toxic metal causing various adverse neurological, developmental, and reproductive disorders. Mercury exposure occurs through contaminated water and food. Ginseng (herbal medicine) can improve male fertility by acting directly on the pituitary gland and central nervous system. Aim of the work The aim of the study was to evaluate the role of Ginseng on mercury chloride-induced testicular toxicity in adult albino rats. Materials and methods Thirty-two adult male albino rats were divided randomly into four groups of eight rats each: group I (the Control group): the animals in this group received 1.5 ml of distilled water; group II (the Ginseng group): the animals in this group received 100 mg/kg body weight of Ginseng; group III (the Mercury Chloride group): the animals in this group received mercury chloride at a dose of 2.0 mg/kg/day. Group IV (the Ginseng and Mercury Chloride group): the animals in this group received both Ginseng and mercury chloride at the same dose and route of administration as the previous group. The testes were removed and fixed. Paraffin sections were prepared and stained with H&E and Masson’s trichrome, and immunohistochemical staining was performed for proliferating cell nuclear antigen. Morphometric study was conducted and results were statistically analyzed. Results The study showed significant increase in body weight in group II and decrease in body weight in groups III and IV compared with the Control group. The gonadal index of group III showed significant decrease compared with both the Control group and group II. H&E sections of group III showed loosely packed vacuolated seminiferous tubules. Some germ cells showed a hyperchromatic nucleus, whereas others showed chromatolysis. Absence of mature sperms was noticed. Some tubules showed massive loss of germ cells. In the treated group (group IV) germ cells regained more or less a normal appearance. Conclusion Ginseng can ameliorate the toxic changes of mercury chloride on the rat testis.

Histological and biochemical studies on the effect of vitamin E on sodium fluoride induced lung toxicity in adult albino rats

Introduction Fluoride compounds are naturally present in soil, water, and food. Furthermore, fluoride in amounts exceeding the standard therapeutic dosage accumulates in hard and soft tissues, where it disturbs the metabolic processes and produces noticeable changes in multiple organs. Aim The study was designed to investigate the effects of sodium fluoride (NaF) on the lung of adult albino rats and the possible protective role of vitamin E on these changes. Materials and methods Twenty-six adult albino rats were divided into three groups: group I (control), group II receiving NaF alone (10 mg/kg body weight), and group III receiving the same NaF dose together with vitamin E supplementation (3 mg/day orally for 35 days). Tissue homogenates were collected for biochemical study, and the lung tissues were excised for histological, immunohistochemical, and biochemical studies. The results of biochemical and immunohistochemical studies were measured and statistically analyzed. Results Lung sections of rats treated with NaF showed congestion and injury in the endothelium of blood vessels, with hemorrhage and injury in the alveolar epithelium. Proliferation of pneumocytes type II and interstitial septal cells were seen. Thickening of interalveolar septum by cellular infiltration and red blood cells with subsequent decrease in the alveolar space was observed. Some area showed compensatory dilated alveolar ducts. A significant increase in the mean area% of cyclooxygenase-2-immunopositive cells was observed when compared with other groups. There was a significant decrease in the catalase activity and an increase in malondialdehyde concentration in group II. In vitamin E-treated group, most fields showed normal lung structure and some fields showed thickened interalveolar septa and dilated air spaces. Conclusion The use of vitamin E has a beneficial effect on the protection of lung against NaF-induced injury.

Role of Protective Effect of L-Carnitine against Acute Acetaminophen Induced Hepatic Toxicity in Adult Albino Rats

Background: Acetaminophen, a widely used analgesic and antipyretic is known to cause hepatic injury in humans and experimental animals when administered in high doses. It was reported that toxic effects of acetaminophen are due to oxidative reactions that take place during its metabolism. L-carnitine is a cofactor in the transfer of long-chain fatty acid allowing to the beta-oxidation of fatty acid in the mitochondria. It is a known antioxidant with protective effects against lipid peroxidation. This study aimed to investigate the possible beneficial effect of L-carnitine as an antioxidant agent against acetaminophen induced hepatic toxicity in rats. Material and Methods: Four rat groups (N=7 in each group). Group I is the control, group II received 500 mg/kg/ body weight of L-carnitine for 7 days by oral route, group III received 640/kg/ bw of acetaminophen by oral route, group IV acute acetaminophen group pretreated with L-carnitine for 7 days by gastric tube gavage tube. The liver of all rats were removed for investigation using light and electro microscopic studies. Results: Acetaminophen caused massive centrilobular necrosis and massive degenerative changes. The electron-microscopic study showed few mitochondria, increased fat droplets and scanty smooth endoplasmic reticulum (SER), rough endoplasmic reticulum (RER).These changes were reduced by L-carnitine pretreatment. Conclusion: those results suggest that acetaminophen results damage in the liver as an acute effect and L-carnitine ameliorated the adverse effects of acetaminophen via its antioxidant role.

Role of Protective Effect of L-Carnitine against Acute Acetaminophen Induced Hepatic Toxicity in Adult Albino Rats

Background: Acetaminophen, a widely used analgesic and antipyretic is known to cause hepatic injury in humans and experimental animals when administered in high doses. It was reported that toxic effects of acetaminophen are due to oxidative reactions that take place during its metabolism. L-carnitine is a cofactor in the transfer of long-chain fatty acid allowing to the beta-oxidation of fatty acid in the mitochondria. It is a known antioxidant with protective effects against lipid peroxidation. This study aimed to investigate the possible beneficial effect of L-carnitine as an antioxidant agent against acetaminophen induced hepatic toxicity in rats. Material and Methods: Four rat groups (N=7 in each group). Group I is the control, group II received 500 mg/kg/ body weight of L-carnitine for 7 days by oral route, group III received 640/kg/ bw of acetaminophen by oral route, group IV acute acetaminophen group pretreated with L-carnitine for 7 days by gastric tube gavage tube. The liver of all rats were removed for investigation using light and electro microscopic studies. Results: Acetaminophen caused massive centrilobular necrosis and massive degenerative changes. The electron-microscopic study showed few mitochondria, increased fat droplets and scanty smooth endoplasmic reticulum (SER), rough endoplasmic reticulum (RER).These changes were reduced by L-carnitine pretreatment. Conclusion: those results suggest that acetaminophen results damage in the liver as an acute effect and L-carnitine ameliorated the adverse effects of acetaminophen via its antioxidant role.

Prophylactic role of β-carotene against acrylonitrile-induced testicular toxicity in rats: Physiological and microscopical studies

Acrylonitrile (ACN) is an aliphatic nitrile product which is extensively used in various synthetic chemical industries. ACN is known to exert toxic actions to human beings as well as experimental animals. The present study was designed to examine the ability of β-carotene, a naturally occurring antioxidant, to attenuate ACN-induced testicular toxicity in adult albino rats. Daily oral administration of ACN at a dose level of 30mg/kg b.w. (7.2mg/animal) to male rats for a period of 5 days significantly reduced the levels of serum testosterone (T), androsterone, follicle-stimulating hormone (FSH) and luteinizing hormone (LH) which indicate injury to the testis function. Also, it decreased serum and testicular glutathione (GSH) content and glutathione-S-transferase (GST) activity. While, ACN induced lipid peroxidation as indicated by markedly increased malondialdehyde (MDA). ACN intoxication also induced marked alterations in most of the seminiferous tubules including germ cell depletion, tubular atrophy, maturation arrest, complete necrosis as well as multinucleated giant cell formation. Expansion of intertubular spaces and interstitial haemorrhage were also illustrated. Ultrastructural examination of the seminiferous tubules revealed thickened boundary tissue, pyknosis of Sertoli cell nuclei, damaged mitochondria and smooth endoplasmic reticulum-derived vacuoles. Spermatogenic cells also demonstrated altered cytoplasmic organelles, vacuoles of varying sizes and deformed spermatids. Mitochondrial disruption and a decrease in the amount of smooth endoplasmic reticulum were observed in Leydig cells. Compared to ACN-treated animals, pretreatment with β-carotene and its co-administration with ACN once daily at a dose of 40mg/kg b.w. (9.6mg/animal) for 30 days induced a remarkable degree of improvement in the levels of endocrine parameters including T, androsterone, FSH and LH. Also, it mitigates serum and testicular GSH content, GST activity and MDA level. Moreover, it protects testicular tissues and cell structures.In conclusion, the present results clearly demonstrate the prophylactic role of β-carotene against ACN-induced testicular toxicity in rats.

Histological and immunohistochemical study on the possible cardioprotective role of acetylcysteine in oral formalin myocardial toxicity in adult albino rats

Histological and immunohistochemical study on the possible cardioprotective role of acetylcysteine in oral formalin myocardial toxicity in adult albino rats