Protective Role Of Ascorbic Acid Research Articles

The protective role of ascorbic acid on the testis tissue damage induced by paracetamol in albino rats

Ascorbic acid (AA) plays roles in many biological functions, such as participating in the production of collagen by taking a role in proline and lysine hydroxylation. AA works by removing the reactive oxygen species, thus removing the adhesion of neutrophils to endothelium. The present study investigates the protective effects of AA on the testis tissue damage induced by paracetamol in rats. Thirty-two male rats were equally divided into four groups, with eight rats in each. Group (1) regular control group, group (2) was received 500 mg/kg/b.w. of AA orally for two weeks, group (3) was received 500 mg/kg/b.w. of paracetamol orally for two weeks, group (4) was treated with the AA (500 mg/kg/b.w.) and paracetamol (500 mg/kg/b.w.) orally for two weeks. The histopathological investigations of the testis tissues from the paracetamol group showed atrophy and degeneration of seminiferous tubules with an absence of spermatozoa, presence of cell debris, and loss of the Sertoli cells in some seminiferous tubules when compared with control animals. The testis tissues from a protective group showed less damage in the tubules and germ cells when compared with the paracetamol group. This study indicates that AA protects against paracetamol-induced testis damage in adult male rats.

In silico and in vitro testing Ascorbic Acid Protects Nicotine-Treated Human Erythrocytes

Objectives: Nicotine is a naturally occurring drug that is highly addictive and is commonly found in tobacco products. Tobacco products are one of the leading causes of lung and oral cancer worldwide. Because blood is the primary organ in contact with nicotine, our goal in this study was to confirm its effect on blood. We also investigated the protective role of ascorbic acid on nicotine toxicity.
 Methods: Various blood toxicity studies were carried out using in-vitro and in-silico methods. Nicotine-induced haematological perturbation resulted in haemolysis, decreased superoxide dismutase and catalase activities, and decreased total antioxidant capacity in erythrocytes.
 Results and Conclusions: The results showed that nicotine has a negative effect on red blood cells in the lysis assay and causes clots to form in nicotine-treated samples in the blood clotting analysis. Furthermore, the in-Silico method validated the in-vitro results. According to our findings, ascorbic acid has blood-protective properties. Ascorbic acid was discovered to increase SOD, catalase, and total antioxidant activity. Ascorbic acid also reduced the damage caused by nicotine to RBCs in the lysis assay and demonstrated a high level of protection against the formation of clots when the samples were treated with nicotine. The findings suggest that ascorbic acid, an antioxidant, can protect against nicotine-induced haematological damage.

In silico and in vitro testing Ascorbic Acid Protects Nicotine-Treated Human Erythrocytes

Objectives: Nicotine is a naturally occurring drug that is highly addictive and is commonly found in tobacco products. Tobacco products are one of the leading causes of lung and oral cancer worldwide. Because blood is the primary organ in contact with nicotine, our goal in this study was to confirm its effect on blood. We also investigated the protective role of ascorbic acid on nicotine toxicity. Methods: Various blood toxicity studies were carried out using in-vitro and in-silico methods. Nicotine-induced haematological perturbation resulted in haemolysis, decreased superoxide dismutase and catalase activities, and decreased total antioxidant capacity in erythrocytes. Results and Conclusions: The results showed that nicotine has a negative effect on red blood cells in the lysis assay and causes clots to form in nicotine-treated samples in the blood clotting analysis. Furthermore, the in-Silico method validated the in-vitro results. According to our findings, ascorbic acid has blood-protective properties. Ascorbic acid was discovered to increase SOD, catalase, and total antioxidant activity. Ascorbic acid also reduced the damage caused by nicotine to RBCs in the lysis assay and demonstrated a high level of protection against the formation of clots when the samples were treated with nicotine. The findings suggest that ascorbic acid, an antioxidant, can protect against nicotine-induced haematological damage.

Ascorbic acid attenuates cadmium-induced myocardial hypertrophy and cardiomyocyte injury through Nrf2 signaling pathways comparable to resveratrol.

Chronic cadmium (Cd) exposure severely affects the structural integrity of the heart, leading to cardiovascular disease. This study investigates the protective role of ascorbic acid (AA) and resveratrol (Res) in cellular defense against Cd-induced cardiomyocyte damage and myocardial hypertrophy in H9c2 cardiomyocytes. Experimental results showed that AA and Res treatment significantly increased cell viability, reduced ROS production, attenuated lipid peroxidation, and increased antioxidant enzyme activity in Cd-induced H9c2 cells. AA and Res decreased the mitochondrial membrane permeability and protected the cells from Cd induced cardiomyocyte damage. This also suppressed the pathological hypertrophic response triggered by Cd, which increased the cell size of cardiomyocytes. Gene expression studies revealed that cells treated with AA and Res decreased the expression of hypertrophic genes ANP (two-fold), BNP (one-fold) and β- MHC (two-fold) compared to Cd exposed cells. AA and Res promoted the nuclear translocation of Nrf2 and increased the expression of antioxidant genes (HO-1, NQO1, SOD and CAT) during Cd mediated myocardial hypertrophy. This study proves that AA and Res play a significant role in improving Nrf2 signaling, thereby reversing stress-induced injury, and facilitating the regression of myocardial hypertrophy.

Protective role of ascorbic acid on lead-induced damage to the thyroid gland in the rat.

Lead exposure is known to affect the pituitary-thyroid axis. Likewise, ascorbic acid (AA) has a protective action against lead poisoning. We examine the protective role of AA in lead-induced damage to the thyroid gland. The Wistar rats were divided into three groups: control that received 0.2% AA in drinking water throughout the experiment (15days), intoxicated with lead acetate (20mg/kg) intraperitoneally every 48h for 15days, and the experimental group treated with lead acetate and 0.2% AA in drinking water throughout the experiment. Plasma thyroid-stimulating hormone, triiodothyronine, thyroxine, and lead were determined. The thyroid gland was weighed, then epithelial cell height and nuclear volume were measured on histological slides. The results show that AA reduced the thyroid atrophy caused by lead acetate, as well as the loss of weight of the gland. In addition, it prevented the decrease of the hormone triiodothyronine, although the thyroxine hormone remained lower than the control values ​​and the thyroid-stimulating hormone remains high. Our results indicated that AA could play a protective role in lead poisoning in the thyroid gland.

Evaluation of the anti-oxidant effect of ascorbic acid on apoptosis and proliferation of germinal epithelium cells of rat testis following malathion-induced toxicity.

Objective(s):The aim of this study was to determine the protective role of ascorbic acid on apoptosis and proliferation of spermatogonia and primary spermatocyte cells after malathion administration as an organophosphate pesticide in rat testis.Materials and Methods:Thirty male Wistar rats were randomly divided into five groups of 6 rats each, including control (no intervention), sham (normal saline 0.09%), malathion (50 mg/kg), malathion plus ascorbic acid (50 mg/kg and 200 mg/kg, respectively), and ascorbic acid (200 mg/kg) groups. Malathion and ascorbic acid were administrated via intraperitoneal injection once per day and seven times per week. After 6 weeks, animals were sacrificed, and testis tissue was used for evaluation of apoptosis and proliferation of germinal epithelium cells using the TUNEL and PCNA staining techniques. Results:The results of TUNEL staining showed that the numbers of apoptotic cells in spermatogonia and primary spermatocyte cells were significantly increased in the malathion 50 mg/kg group vs control group (P<0.001). Co-administration of malathion 50 mg/kg and ascorbic acid 200 mg/kg significantly decreased the apoptotic cells in both cell types in comparison with malathion 50 mg/kg group (P<0.001). The results of PCNA staining revealed that the proliferation of these cells was significantly decreased in malathion 50 mg/kg group vs control group (P<0.001), and malathion 50 mg/kg plus ascorbic acid 200 mg/kg administration increased the proliferation of cells compared with malathion 50 mg/kg group (P<0.001).Conclusion:The results provide evidence that ascorbic acid showed preventive effects on malathion-induced toxicity in male rat testis.

Possible Ameliorating Role of Ascorbic Acid on Intestinal Changes Induced by Acrylamide in Adult Female Albino Rats and Their Offsprings

Background: Acrylamide (ACR) is a naturally occurring, widely used compound. Ingestion of large amounts of ACR underlies several health concerns and teratogenicity. Ascorbic acid (vitamin C) is a strong reducing agent greatly used to clean free radicals. This study investigated the morphometric, histological, immunohistochemical and biochemical disturbances induced by acrylamide (10 mg/kg/day) via gavage in the intestine of rat mothers and their offsprings. As well as, the protective role of ascorbic acid (100 mg/kg/day) via gavage.Materials and Methods: Forty adult pregnant female rats were divided into four groups; control, ascorbic acid, acrylamide and acrylamide+ascorbic acid. 10 randomly chosen offsprings of each group after weaning were also used. Histomorphometric analysis of intestinal wall and biochemical analysis of intestinal enzymes, oxidant antioxidant markers and some genes expression were performed.Results: In both dams and offsprings, ACR resulted in mucosal hyperplasia with evident inflammatory infiltration in the villi. In addition, goblet cells and KI67 +ve cell numbers decreased in the dams however increased in offsprings. ACR decreased citrate synthase, glutathione and catalase levels in dams and increased β-glucuronidase and malonaldehyde levels in dams. In offsprings, level of alkaline phosphatase was reduced and β-glucuronidase was elevated. Glutathione peroxidase and glutathione reductase mRNA expression was increased significantly with ACR ingestion. Ascorbic acid supplementation conserved the control status in the majority of conditions.Conclusion: Acrylamide consumption during pregnancy and lactation is risky because of the induction of intestinal mucosal hyperplasia in rat offsprings. Ascorbic acid supplementation could reduce the harmful effects induced by ACR.

Effect of ultrasound on rabbit cornea and the protective role of antioxidant

Background/aim Applications of ultrasound in medicine for therapeutic purposes have been an accepted and beneficial use for many years. The present study aimed to investigate the harmful effect of exposure to therapeutic ultrasound on the cornea and the possible protective role of ascorbic acid and β-carotene. Materials and methods A total of 50 healthy mature New Zealand albino rabbits were enrolled in this study and classified into four groups. Group I contained five rabbits and were used as a control group. The remaining rabbits were classified into three groups of fifteen rabbits each. The eyes of group II were insonificated with continuous ultrasound waves (1.5 W/cm2 at 2.8 MHz) for 20, 40, and 60 min. Group III and group IV were topically treated with vitamin C and supplemented with β-carotene, respectively, before insonificated with ultrasound for 20, 40, and 60 min. All the rabbits were decapitated 24 h after ultrasound exposure. Total soluble protein content and Fourier-transform infrared (FTIR) analyses were carried out on cornea. Results Soluble protein content of cornea recorded highly significant decreased (P Conclusion Ultrasound waves have the possibility to cause significant change in the molecular structure of corneal tissue. The use of antioxidants such as vitamin C and β-carotene preserves the corneal tissue, especially at short insonification time.

Possiple Protective Role of Ascorbic Acid on Ethanol Induced Testicular Toxicity in Male Albino Rats

Background: Exposure to ethanol results in many pathophysiologic changes in the function of the reproductive system caused by the alcohol itself and the effects of its metabolism in recurrent use. Ascorbic acid is a powerful antioxidant that can neutralize harmful compounds and potentiate the antioxidant capacity. Aim: this study was aimed to evaluate the protective effects of ascorbic acid against testicular changes caused by ethanol in adult male albino rats. Materials and Methods: Forty adult male rats were randomly distributed into four groups treated for 63 consecutive days, control group: was treated with distilled water only orally by gastric tube. Ascorbic acid group: was treated with ascorbic acid (100 mg/day/rat) dissolved in distilled water (dilution 50%), once daily orally by gastric tube. Ethanol group: was treated with ethanol (0.7g/kg) dissolved in distilled water (dilution 50% ), once daily orally by gastric tube. Ethanol and ascorbic acid group: was treated with ethanol and ascorbic acid in the same previous doses orally by gastric tube. At the end of the study, rats were weighed then blood samples were obtained from each group to estimate the level of testosterone. Then the rats were sacrificed. The testes were dissected and weighed then used for evaluation of oxidative parameters (GSH and MDA), histopathological examination of testes by light and electron microscope. Results: Concomitant administration of ascorbic acid with ethanol resulted in a highly significant rise in body weight, with increase in mean testosterone level but this rise was insignificant, there was a highly significant decrease in MDA level and there was a highly significant increase in GSH level. Regarding histopathological results in the group of ascorbic acid with ethanol showed improvement in all histopathological changes induced by ethanol. As regard ultrastructure changes, microscopic examination in ethanol group revealed thickening of basement membrane, mitochondrial changes, degenerated spermatid, with decrease in the sperm count results which were improved in the group of ascorbic acid with ethanol. Conclusion: oral administration of ethanol daily for 63 consecutive days in adult albino rats caused various testicular lesions which were significantly reduced with combined administration of ascorbic acid as antioxidant

Deleterious Effect of Maternal administration of Acrylamide on Lung Development and the Prospective Effect of Ascorbic Acid: Pertinent Role of Serum Endocan

Introduction: Acrylamide (ACR) is an environmental pollutant that is present in surrounding environment and Western-style carbohydrate-rich foodstuff and tobacco smoke.Aim of the Study: The aim of the study was to assess the potential histological changes in the lung of nascent rats as a consequence to maternal ACR administration and the possible protective role of ascorbic acid (ASA) in rat offspring.Materials and Methods: Pregnant rats were randomly assigned into four groups, negative control group, ASA group (100 mg/kg/day), ACR group (10 mg/kg/day) and ACR+ASA group. Ten pups from each group were sacrificed. Biochemical, histological and morphometric techniques were used to determine the effect of ACR and ASA on lung development in the offspring on postnatal days (PND) 2 and 21.Results: The results showed that ACR administration during gestational and lactation periods significantly increased the serum endocan and the lung malondialdehyde (MDA) but decreased the lung reduced glutathione (GSH) along with severe histopathological changes proved ultra-structurally. Morphometric results revealed significant increase thickness in interalveolar septa among ACR group. Concurrent administration of ASC with ACR during gestation period attenuated most of the cytoarchitecture alterations of the developing lungs.Conclusion: Maternal administration of acrylamide resulted in harmful impact on the lung histological structure of rat's offspring through its oxidative stress and inflammatory mechanisms. Co-administration of ASA along with ACR can ameliorate this deleterious impact through its antioxidant and anti- inflammatory properties

Oxidative stress mitigation and initiation of antioxidant and osmoprotectant responses mediated by ascorbic acid in Brassica juncea L. subjected to copper (II) stress

Copper (Cu) is an essential yet toxic metal, which holds the ability to induce production of reactive oxygen species (ROS) in living cells resulting in severe abiotic stress. Therefore, the aim of our current study was to investigate the effects of extrinsically added ascorbic acid (AA) on oxidative stress indicators and redox homoeostasis remediators in 7-day-old seedlings and 60-day-old plants of Brassica juncea L. (hyper-accumulator species) subjected to Cu (II) stress. Our findings showed that seed germination ballooned by 55.4% in Cu (II) stressed seedlings upon addition of 50 mg l−1 AA. Copper content accelerated in stressed seedlings and plants; however, a negative interaction was seen upon addition of AA. Both seedlings and plants exposed to Cu (II) accumulated free radicals such as H2O2 and superoxide anion, however, the addition of AA in the growth media decreased H2O2 and superoxide anion generation indicating ROS detoxification. Confocal microscopy also revealed improved cell viability and reduced H2O2 content because of enhanced antioxidant activity upon addition of AA as a protective chelate. Antioxidants such as ascorbate, flavonoids and glutathione rose significantly in Cu (II) stressed seedlings and plants in the presence of AA. Protein content increased by 51.3% and 47.5% in seedlings and plants growing in a binary combination of 100 mg l−1 Cu and AA (75 mg l−1 and 25 mg l−1), respectively. Sharp peaks for stress indicator amino acids such as cysteine and proline were seen in spectral analysis of B. juncea seedlings exposed to Cu (II). Protein thiols increased in plants grown in various binary doses Cu (II) and AA. This study provides sufficient evidence regarding the protective role of ascorbic acid (AA) against ROS and its suggested use as a soil amendment against Cu (II) toxicity in B. juncea.

The protective role of ascorbic acid in the hepatotoxicity of cadmium and mercury in rabbits

The liver is one of the vital and sensitive organs which are usually exposed against the toxicity of mercury (Hg) and cadmium (Cd). The main objective of the current study was to evaluate the potential toxicological effects of both Cd and Hg as individual and combined. Hepatotoxicity was evaluated by monitoring the biochemical parameters of the liver and their accumulation in the liver as well as therapeutic role of vitamin C in said toxicity in rabbits (Oryctolagus cuniculus). In this research, cadmium chloride (1.5 mg/kg), mercuric chloride (1.2 mg/kg), and vitamin C (150 mg/kg of body weight) were orally administered to treatment groups of the rabbits for 28 alternative days. Various biochemical parameters of the liver such as lactate dehydrogenase (LDH), aspartate aminotransferase (ASAT), bilirubin, alanine aminotransferase (ALAT), total protein, and gamma glutamyl transferase (GGT) were estimated using blood samples. Some biochemical parameters like ASAT, ALAT, LDH, GGT, and bilirubin were significantly elevated (P ≤ 0.001) in individual Cd and Hg treatment groups, while the level of total protein was found to be significantly declined. The effects of Cd and Hg in the presence of vitamin C on these biochemical parameters were low as compared to metals-treated groups. Similar results were found when rabbits were treated with co-administration of both metals and vitamin C. Accumulation of Cd and Hg found to be higher in the liver. However, chemoprevention and chemotreatment with vitamin C significantly (P ≤ 0.01) minimized the toxicological effects of both metals but not regained the accumulation similar to that of the control group. The findings of this study provide awareness on accumulation of metals in the liver in rabbits and their toxicity tested through biochemical parameters as well as the therapeutic role of vitamin C in such alterations.

Evaluating the Protective Role of Ascorbic Acid in Malathion-induced Testis Tissue Toxicity of Male Rats.

Background:Malathion is one of organophosphate pesticides that is widely used in agriculture and crops to control insects. Malathion affects body organs such as the reproductive system by inhibiting acetylcholinesterase activity and induction of oxidative stress. This study is aimed to investigate the effects of malathion on glutathione (GSH) and malondialdehyde (MDA) level in testis of male rats, as well as to study the protective role of Ascorbic Acid.Methods:In this study, 30 adult male Wistar rats weighing approximately 200–250 g were divided into 5 groups of 6 rats each. These groups include a control group (no intervention), sham (normal saline 0.9%), experimental Group 1 (malathion 50 mg/kg), experimental Group 2 (Malathion 50 mg/kg + Ascorbic Acid 200 mg/kg), and experimental Group 3 (Ascorbic Acid 200 mg/kg). Malathion, solvents, and ascorbic acid were injected intraperitoneally. After 6 weeks, all groups were anesthetized, and the right testis was used to measure levels of MDA and GSH. MDA as a marker of lipid peroxidation and GSH content was used.Results:The results showed that malathion increased MDA level and decreased GSH level compared with the control group (P < 0.001). It was also found that administration of malathion in combination with ascorbic acid reduced MDA level and increased the GSH level.Conclusions:Malathion-induced lipid peroxidation and oxidative stress in the testis of rats. In addition, it seems that ascorbic acid, due to its antioxidant capabilities, can improve malathion-induced poisonous changes.

Protective role of ascorbic acid on testiculotoxic effect induced by allethrin based mosquito coil smoke

Protective role of ascorbic acid on testiculotoxic effect induced by allethrin based mosquito coil smoke

The protective role of ascorbic acid on hippocampal CA1 pyramidal neurons in a rat model of maternal lead exposure

Oxidative stress is a major pathogenic mechanism of lead neurotoxicity. The antioxidant ascorbic acid protects hippocampal pyramidal neurons against cell death during congenital lead exposure; however, critical functions like synaptic transmission, integration, and plasticity depend on preservation of dendritic and somal morphology. This study was designed to examine if ascorbic acid also protects neuronal morphology during developmental lead exposure. Timed pregnant rats were divided into four treatment groups: (1) control, (2) 100mg/kg ascorbic acid once a day via gavage, (3) 0.05% lead acetate in drinking water, and (4) 0.05% lead+100mg/kg oral ascorbic acid. Brains of eight male pups (P25) per treatment group were processed for Golgi staining. Changes in hippocampal CA1 pyramidal neurons’ somal size were estimated by cross-sectional area and changes in dendritic arborization by Sholl’s analysis. One-way ANOVA was used to compare results among treatment groups. Lead-exposed pups exhibited a significant decrease in somal size compared to controls (P<0.01) that was reversed by cotreatment with ascorbic acid. Sholl’s analysis revealed a significant increase in apical dendritic branch points near cell body (P<0.05) and a decreased total dendritic length in both apical and basal dendritic trees of CA1 neurons (P<0.05). Ascorbic acid significantly but only partially reversed the somal and dendritic damage caused by developmental lead exposure. Oxidative stress thus contributes to lead neurotoxicity but other pathogenic mechanisms are also involved.

Histological Study on the Protective Role of Ascorbic Acid on Cadmium Induced Cerebral Cortical Neurotoxicity in Adult Male Albino Rats

Cadmium (Cd) toxicity represents a worldwide problem in environmental contamination and a common cause of occupational and non-occupational neurological diseases. So, this study aimed to evaluate the histological changes induced by Cd on the cerebral cortex of adult rats and evaluating the possible ameliorating role of ascorbic acid (AA). Twenty adult male rats were divided into; control group, AA group (each rat was received a daily oral dose of 200mg AA/kg body weight (b.w) and Cd group (each rat was received 5mg Cd/kg b.w orally) and protective group (each rat was given AA concomitantly with Cd at the same dose, route and period of administration of the previous groups. After two months the cerebral cortexes were processed for histological examination. The cerebral cortex of Cd treated animals exhibited severe degenerative changes especially in pyramidal and granule cells. Structural changes in these cells were in the form of dilated rER and Golgi complex, swollen mitochondria and marginated nuclear chromatin. Myelinated nerve fibers displayed myelination disruption and irregular neurofilaments. The neuropil appeared vacuolated with accumulation of neuroglial cells. On the other hand, these changes were ameliorated in rats which received AA concomitantly with Cd. So, it could be concluded that AA can ameliorate the histological changes induced by Cd and this direct the attention to the antioxidants as protective measures for the neurotoxicity.

Biochemical changes associated with ascorbic acid–cisplatin combination therapeutic efficacy and protective effect on cisplatin-induced toxicity in tumor-bearing mice

Cisplatin is one of the well-established anticancer drugs being used against a wide spectrum of cancers. However, full therapeutic efficacy of the drug is limited due to development of various toxicities in the host. This study examines the comparative therapeutic effectiveness and toxicities of cisplatin alone and in combination of dietary ascorbic acid (AA) in ascites Dalton's lymphoma-bearing mice. The findings show that the combination treatment of mice with ascorbic acid plus cisplatin has much better therapeutic efficacy against murine ascites Dalton's lymphoma (DL) in comparison to cisplatin alone and this may involve a decrease in reduced glutathione (GSH), catalase activity and increased lipid peroxidation (LPO) in Dalton's lymphoma tumor cells. At the same time, combination treatment indicates a protective role of ascorbic acid against cisplatin-induced tissue toxicities (side effects) in the hosts. Cisplatin-induced histopathological changes in liver, kidney and testes were decreased after combination treatment. The analysis of renal function test (RFT), liver function test (LFT) and sperm abnormalities also suggest an improvement in these parameters after combination treatment. Therefore, it may be concluded that the increased GSH level, catalase activity and decreased LPO in the tissues, i.e., liver, kidney and testes after combination treatment may be involved in its protective ability against cisplatin-induced tissue toxicities in the host.

Oxidative Stress Biomarkers in the Freshwater Fish, Heteropneustes fossilis (Bloch) Exposed to Sodium Fluoride: Antioxidant Defense and Role of Ascorbic Acid.

The present study highlights fluoride -induced toxicity and the protective role of ascorbic acid in the liver and ovary of freshwater fish, Heteropneustis fossilis. The fish specimens were exposed to different concentrations (35 mg F/L and 70 mg F/L) of fluoride. Parameters related to oxidative stress were studied at the end of the experiment. The biomarkers selected for the study were thiobarbituric acid reactive substances for assessing the extent of lipid peroxidation (LPO) and antioxidant defense system such as reduced glutathione (GSH), superoxide dismutase (SOD) catalase (CAT) glutathione peroxidase (GPx), and glutathione S-transferase (GST) activities. The fluoride exposure significantly elevated the level of LPO, CAT, SOD, and GST in the tissues of treated group as well as modulated the activities of GSH and level of GPx after exposure as compared to the control. A significant decrease in GPx activity was found in these tissues suggesting that fluoride exposure increases the level of free radical, as well as CAT activity. Pre- and post treatment with ascorbic acid decreased the LPO, SOD, CAT, GST level, and increased GSH, GPx levels in the liver and ovary.

Phenthoate induced-oxidative stress in fresh isolated mice hepatocytes: Alleviation by ascorbic acid

This study was conducted to determine the protective role of ascorbic acid (AA) against cytotoxicity of the phenthoate (PTA) on hepatocytes. Lipid peroxidation (LPO), nitric oxide (NO), antioxidant enzymes like superoxide dismutase, catalase, glutathione peroxidase, gamma glutamyl transferase and glutathione-S-transferase activities were measured. Non-enzymes antioxidant levels of reduced glutathione (GSH), ferric reducing antioxidant power (FRAP), AA and total proteins (TP) were determined. The results were demonstrated that the 2 hr-LC50 obtained for PTA value was 79.94 mM. LPO and NO were increased in hepatocytes-treated with PTA. PTA-induced oxidative stress in the isolated hepatocytes by decreasing the levels of some antioxidant enzymes. GSH levels were also diminished in PTA treated-hepatocytes as compared to DMSO hepatocytes. FRAP, AA and total protein were also decreased following treatment with PTA. These findings suggest that cytotoxicity of PTA is mediated by increasing free radical formation and decreasing the antioxidants. PTA hepatotoxicity increased in a time- and concentration-dependent manner. The AA can be very effective in perhaps reducing the extent of injury and in overcoming oxidant damage caused by PTA.

Thyroxine-induced cardiac hypertrophy: Role of ascorbic acid in treatment

The heart is a major target organ for thyroid hormone action and marked changes occur in cardiac function in the case of hypo- or hyperthyroidism. Hyperthyroidism is a common metabolic disorder with prominent cardiovascular manifestation. We studied the changes in the heart structure and functions of hyperthyroid rat and ameliorating and protective role of ascorbic acid in treatment. Fourty male albino rats were equally divided into five groups; the first and second groups were the control and ascorbic acid groups respectively. Third group was the hyperthyroid rat group while 4th and 5th groups were co- and post-treated hyperthyroid rat with ascorbic acid respectively. Serum T3 and T4 levels were significantly increased also; TSH levels were significantly decreased in hyperthyroid rat as compared to control rat groups. Cholesterol, triglyceride, LDL-c and VLDL-c were significantly decreased when compared with control group. Many of abnormalities as severe hydrophobic changes of myofibrillar structure with striations, hypertrophy, cytoplasmic vacuoles and marked increase in desmin immunoreactivity were observed in left ventricle in hyperthyroid rats. Treatment with ascorbic acid helps in improving the adverse effect of hypothyroidism and also the histopathological and desmin immunoreactivity results confirms this finding.