Protective Effect Of Ascorbic Acid Research Articles

Protective Effects of Ascorbic Acid Against Cadmium-Induced Toxicity in the Placenta and Fetus of Rats.

This study aimed to determine the protective role of l-ascorbic acid in a pregnant rat model of cadmium-induced toxicity. Cadmium is a toxic heavy metal that can seriously harm placenta and fetus tissue in pregnant women. Forty-two healthy female Wistar albino rats (250-300 g weight and 14-16 weeks) were randomly distributed into six equal groups (n = 7): control, cadmium 1 mg (CD1), cadmium 5 mg (CD5), ascorbic acid (AA), CD1+AA, CD5+AA. Cadmium was administered to pregnant rats by oral gavage every other day, and/or AA (200 mg) was administered every day. At the end of pregnancy (Day 21), blood, placenta, and fetuses were collected from rats. The results indicated that cadmium-induced oxidative stress by increasing the level of MDA and by decreasing the levels of GSH, SOD, and CAT activity in the serum of maternal. However, AA administration significantly decreased MDA levels and increased GSH levels, SOD, and CAT activity (p < 0.05). Cadmium (5 mg/kg) exposure significantly increased creatinine levels compared to AA and CD1+AA groups (p < 0.05). In addition, AA (200 mg/kg) significantly attenuated cadmium-induced histopathological alteration in the placental and fetal tissues. In conclusion, AA may prevent cadmium toxicity in maternal and fetal tissues, as it regulates oxidative imbalance in pregnant rat tissues and alleviates histopathological changes.

Investigating the Protective Effects of Ascorbic Acid Against Paracetamol-induced Liver Toxicity in Wistar Rats

Paracetamol is one of the most widely used analgesics and antipyretics but can cause severe liver damage at high doses. This study explores the potential protective effects of ascorbic acid (vitamin C) against paracetamol-induced hepatotoxicity in Wistar rats. For this experimental study, 25 mature male Wistar rats, weighing 140–180g, were divided into five groups: Group 1 stands for the Normal Control. Group 2 received 25 mg of PCM for 21 days, whereas Group 3 received 500 mg of ascorbic acid. Furthermore, after PCM was given, rats in groups 4 and 5 were given 500 mg and 1000 mg of ascorbic acid, respectively. Following PCM and Ascorbic acid treatment, biochemical parameters and histoarchitectural studies were examined. Histopathological examination of liver tissue was performed to evaluate cellular architecture and damage. Results indicated that treatment with ascorbic acid significantly mitigated the elevation of liver enzymes and histopathological changes compared to the paracetamol-only group. In conclusion, the research underscores the potential role of ascorbic acid in safeguarding liver function.

Ascorbic acid attenuates gasoline-induced testicular toxicity, sperm quality deterioration, and testosterone imbalance in rats.

The present study evaluated the protective effect of ascorbic acid (ASCB) against gasoline fumes (PET) induced testicular oxidative stress, sperm toxicity, and testosterone imbalance in Wistar rats. Twenty-four (24) male albino rats (75 ± 16g) were randomized into three experimental groups (N = 8). The control group: received normal saline, PET group: exposed to PET 6h daily by inhalation in an exposure chamber and PET + 200mg ASCB/kg body weight group: exposed to PET 6h daily by inhalation and administered ASCB per os. Treatment of ASCB and PET exposure was done thrice and five times weekly for a period of 10weeks respectively. ASCB co-treatment prevented PET-induced increases in the oxidative stress markers (glutathione, glutathione S-transferase, superoxide dismutase, catalase, hydrogen peroxide generation, nitric oxide, and lipid peroxidation) and serum testosterone concentration (p < .05). Sperm quality was low and those with damaged heads and tails increased alongside histological injuries in the PET-exposed rats, which were also minimized with ASCB administration. ASCB protected against PET-induced oxidative stress, sperm, and testis damage in rats.

Study on the characterization of 6S-5-methyltetrahydrofolate calcium salt crystal form C and its stability improvement by ascorbic acid and cysteine

6S-5-methyltetrahydrofolate calcium salt crystal form C (MTHF-CAC) is a stable form of active folate. Compared with folic acid, MTHF-CAC is unaffected by the polymorphism of genes for folate-metabolizing enzymes and can be directly absorbed by the human body. In this study, MTHF-CAC was characterized by XRD, FTIR, DSC, and TGA. The effects of temperature, light, pH, and freeze–thaw cycles on the stability of MTHF-CAC solution were studied. The protective effects of ascorbic acid (AA) and cysteine (Cys) on MTHF-CAC were investigated by HPLC. The retention rate of MTHF-CAC solution was 82.6% after 6 days of storage at 4 °C but only 0.8% after heating at 75 °C for 330 min. Under UHT conditions, AA and Cys exerted protective effects on MTHF-CAC. 120 μg/mL of AA and Cys increased the retention of MTHF-CAC by 89.9% and 85.3%, respectively. The protective effect of AA was better than that of Cys. The research on the characterization and stability of MTHF-CAC provided the basic information for its application in the food industry.

In vitro and in silico Protective Effects of Ascorbic Acid on Nicotine-treated Human Erythrocytes (Preliminary Studies)

In vitro and in silico Protective Effects of Ascorbic Acid on Nicotine-treated Human Erythrocytes (Preliminary Studies)

Ascorbic acid modulates testicular toxicity of Ampligo® 150 ZC insecticide in male rabbit (Oryctolagus cuniculus)

The present study was designed to evaluate the protective effects of ascorbic acid (AA) against lambda cyhalothrin insecticide formulation Ampligo® (AP)-induced testicular toxicity in rabbit laboratory strain ITELV2006 (Oryctolagus cuniculus). Twenty rabbits were randomly divided into four equal groups and treated by oral gavage for 21 consecutive days: Group 1 served as a control and received 1 ml of distilled water, group 2 was supplemented with1ml of ascorbic acid (AA) dilution (200 mg/kg b.w), Group 3 was treated with a dose of AP at 20 mg/kg bw (1 µl/1 ml of distilled water/animal), whereas group 4 was co-administered AA and AP as the same dose of group 2 and 3, respectively. Hormonal, histomorphometrical, and immunohistochemical methods were performed at the end of the study to detect testes damage. The results showed that AP exposure significantly reduced body weight, absolute and relative testicular weights, and testosterone levels. AP caused changes in testes tissue, namely incomplete spermatogenic series and necrosis of the spermatogonial cells lining in the seminiferous tubules of rabbits. Co-administrating AA clearly modulated body and testes weights, hormonal parameters, and histopathological damage. Furthermore, the findings revealed a significant increase in alpha-fetoprotein (AFP) level expression in the testes of the AP group. However, supplementation of the AP rabbits with AA modulated the observed result. Taken together, these data suggest that AA may protect against Ampligo-induced testicular damage.

Rapid and sensitive determination of ascorbic acid based on label-free silver triangular nanoplates

In this study, a new method for the detection of ascorbic acid (AA) was proposed. It was based on the protective effect of AA on silver triangular nanoplates (Ag TNPs) against Cl− induced etching reactions. Cl− can attack the corners of Ag TNPs and etch them, causing a morphological shift from triangular nanoplates to nanodiscs. As a result, the solution changes color from blue to yellow. However, in the presence of AA, the corners of Ag TNPs can be protected from Cl− etching, and the blue color of the solution remains unchanged. Using this effect, a selective sensor was designed to detect AA in the range of 0–40.00 μM with a detection limit of 2.17 μM. As the concentration of AA varies in this range, color changes from yellow to blue can be easily observed, so the designed sensor can be used for colorimetric detection. This method can be used to analyze fruit juice samples.

Effects of different concentrations of ascorbic acid on the stability of (+) – Catechin under enzymatic conditions

A series of incubation systems of (+) - catechin (Cat), ascorbic acid (AA) and polyphenol oxidase (PPO) of lotus rhizome at 40 °C were performed to investigate the effect and oxidation pathway of AA on the stability of Cat. The results showed that after the enzymatic or non-enzymatic oxidation of Cat, the products of the two reactions were the same, namely epicatechin, catechin dimer and dehydrogenated catechin dimer. After adding AA, the protective effect of AA on catechin increased first and then decreased with the increase of AA concentration. 0.1 mmolL(exp)-1 AA can inhibit PPO activity in a short time. Within 24 h, 1 mmolL(exp)-1 AA can keep Cat content at 87.88 %. At the concentration of 10 mmolL(exp)-1 AA, excessive AA is oxidized to form a large amount of dehydroascorbic acid (DHAA), which forms an adduct with Cat, promoting the consumption of Cat. The effect of AA on the stability of Cat is time-dependent and dose-dependent.

Effect of Clomiphene Citrate on the Kidney of Female Albino Rat and the Possible Protective Effect of Ascorbic Acid (Light and Electron Microscopic Study)

Effect of Clomiphene Citrate on the Kidney of Female Albino Rat and the Possible Protective Effect of Ascorbic Acid (Light and Electron Microscopic Study)

Ascorbic acid 2-glucoside: An ascorbic acid pro-drug with longer-term antioxidant efficacy in skin.

Deleterious effects of pollutants and ultraviolet radiation on the skin can be attenuated using formulations containing antioxidants. However, these have disadvantages, including chemical instability, photodegradation, poor bioavailability or biological activity. Here, two commercial formulations were evaluated: one optimized to stabilize and deliver ascorbic acid (AA) at 15% and the other containing a glucoside form of AA, namely ascorbic acid 2-glucoside (AA2G), at 1.8% and at a physiological pH. We compared the skin delivery, antioxidative effects and chemical stability of AA2G with AA in their respective formulations. Skin delivery was measured using fresh viable human skin explants, and oxidative stress was measured using a human reconstructed epidermal (RHE) model according to levels of malondialdehyde (MDA), superoxide dismutase (SOD) and catalase. Ascorbic acid 2-glucoside was completely metabolized to AA by the skin before entering the receptor compartment. The skin contained parent and AA, indicating a reserve of AA2G was present for further metabolism. For AA2G and AA, maximum flux of AA-equivalents was at 12h, with continued absorption over 24h. The absolute amount in µg was higher in the skin after application of AA than after application of AA2G. This may suggest a greater antioxidative effect; however, according to all three measurements of oxidative stress, the protective effect of AA and AA2G was similar. Unlike AA, AA2G was chemically stable under storage conditions. A lower concentration of AA2G is as effective as the active metabolite, AA, in terms of antioxidant effects. AA2G was chemically stable and can be applied at a lower concentration than AA, thus avoiding the need for an acidic formulation with a pH below 3.5.

Ultrasonic degradation kinetics and isomerization of 3- and 4-O-caffeoylquinic acid at various pH: The protective effects of ascorbic acid and epigallocatechin gallate on their stability

Caffeoylquinic acids are existed in many plant species with various biological and pharmacological activities. 3-O-caffeoylquinic acid and 4-O-caffeoylquinic acid are two isomers of caffeoylquinic acids, which may be degraded and transformed to their isomers in processing. The present paper found that the stability of 3- and 4-O-caffeoylquinic acid had decreased with the increasing solution alkalinity. 3-O-caffeoylquinic acid was more stable than 4-O-caffeoylquinic acid at the same condition. During degradation, 3- and 4-O-caffeoylquinic acid were partially converted to their isomers. Additionally, ultrasonic effects on the degradation and isomerization of 3- and 4-O-caffeoylquinic acid at different pH were studied. Ultrasound facilitated the degradation and isomerization of these compounds. The degradation kinetics were described by the Weibull equation. The protective effect of ascorbic acid and epigallocatechin gallate were also explored. Ascorbic acid and epigallocatechin gallate could alleviate the degradation of 3- and 4-O-caffeoylquinic acid under certain conditions.

Ultrasonic Degradation Kinetics and Isomerization of 3- and 4-O-Caffeoylquinic Acid at Various Ph: The Protective Effects of Ascorbic Acid and Epigallocatechin Gallate on Their Stability

Caffeoylquinic acids have been found in many plant species with various biological and pharmacological activities. 3- O -caffeoylquinic acid and 4- O -caffeoylquinic acid are two isomers of caffeoylquinic acids, which may be degraded in processing. The present paper found that the stability of 3- and 4- O -caffeoylquinic acid had decreased with the increasing solution alkalinity , while 3- O -caffeoylquinic acid was more stable than 4- O -caffeoylquinic acid at the same condition. 3- and 4- O -caffeoylquinic acid were converted more to each other than to 5- O -caffeoylquinic acid. Additionally, ultrasonic effects on the degradation and isomerization of 3- and 4- O -caffeoylquinic acid at different pH were studied. Ultrasound facilitated the degradation and isomerization of these compounds. The degradation kinetics were described by the Weibull equation. The protective effect of ascorbic acid and epigallocatechin gallate were also explored. Ascorbic acid and epigallocatechin gallate could abate the degradation of 3- and 4- O -caffeoylquinic acid under certain conditions.

Role of ascorbic acid in the regulation of epigenetic processes induced by Porphyromonas gingivalis in endothelial-committed oral stem cells

Periodontitis is a common inflammatory disease that affects the teeth-supporting tissue and causes bone and tooth loss. Moreover, in a worldwide population, periodontal disease is often associated with cardiovascular diseases. Emerging studies have reported that one of the major pathogens related to periodontitis is Porphyromonas gingivalis (P. gingivalis), which triggers the inflammatory intracellular cascade. Here, we hypothesized a possible protective effect of ascorbic acid (AA) in the restoration of the physiological molecular pathway after exposure to lipopolysaccharide derived from P. gingivalis (LPS-G). In particular, human gingiva-derived mesenchymal stem cells (hGMSCs) and endothelial-differentiated hGMSCs (e-hGMSCs) exposed to LPS-G showed upregulation of p300 and downregulation of DNA methyltransferase 1 (DNMT1), proteins associated with DNA methylation and histone acetylation. The co-treatment of AA and LPS-G showed a physiological expression of p300 and DNMT1 in hGMSCs and e-hGMSCs. Moreover, the inflammatory process triggered by LPS-G was demonstrated by evaluation of reactive oxygen species (ROS) and their intracellular localization. AA exposure re-established the physiological ROS levels. Despite the limitations of in vitro study, these findings collectively expand our knowledge regarding the molecular pathways involved in periodontal disease, and suggest the involvement of epigenetic modifications in the development of periodontitis.

RETRACTED ARTICLE: The role of ascorbic acid combined exposure on Imidacloprid-induced oxidative stress and genotoxicity in Nile tilapia

Imidacloprid (Imid), a systemic neonicotinoid insecticide, is broadly used worldwide. It is reported to contaminate aquatic systems. This study was proposed to evaluate oxidative stress and genotoxicity of Imid on Nile tilapia (Oreochromis niloticus) and the protective effect of ascorbic acid (Asc). O. niloticus juveniles (30.4 ± 9.3 g, 11.9 ± 1.3 cm) were divided into six groups (n = 10/replicate). For 21 days, two groups were exposed to sub-lethal concentrations of Imid (8.75 ppm, 1/20 of 72 h-LC50 and 17.5 ppm, 1/10 of 72 h-LC50); other two groups were exposed to Asc (50 ppm) in combination with Imid (8.75 and 17.5 ppm); one group was exposed to Asc (50 ppm) in addition to a group of unexposed fish which served as controls. Oxidative stress was assessed in the liver where the level of enzymatic activities including superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPX) in addition to mRNA transcripts and, Lipid peroxidation (LPO) were evaluated. Moreover, mitotic index (MI) and comet assay were performed, in addition, the erythrocytic micronucleus (MN), and nuclear abnormalities (NA) were observed to assess genotoxicity in fish. Imid exposure induced significant (p ˂ 0.05) changes in the antioxidant profile of the juveniles' liver by increasing the activities and gene expression of SOD, CAT and GPX as well as elevating the levels of LPO. DNA strand breaks in gill cells, erythrocytes and hepatocytes along with erythrocytic MN and NA were also significantly elevated in Imid-exposed groups. MI showed a significant (p ˂ 0.05) decrease associated with Imid exposure. Asc administration induced a significant amelioration towards the Imid toxicity (8.75 and 17.5 ppm). A significant protective potency against the genotoxic effects of Imid was evidenced in Asc co-treated groups. Collectively, results highlight the importance of Asc as a protective agent against Imid-induced oxidative stress and genotoxicity in O. niloticus juveniles.

Caenorhabditis elegans to Model the Capacity of Ascorbic Acid to Reduce Acute Nitrite Toxicity under Different Feed Conditions: Multivariate Analytics on Behavioral Imaging.

Nitrocompounds are present in the environment and human diet and form part of vegetables and processed meat products as additives. These compounds are related to negative impacts on human and animal health. The protective effect of ascorbic acid has been demonstrated by some biological systems as regards several nitrocompounds. This work focused on studying the possibility of modeling this effect on nitrite toxicity with the model Caenorhabditis elegans. The three factors studied in this work were ascorbic acid concentration, nitrite exposure concentration, and presence/absence of food. The protective effect was evaluated by scoring lethality and its impact on behavior by means of multivariate statistical methods and imaging analytics. The effects of nitrite and the influence of food availability were evidenced. Apart from increasing lethality, nitrite had disruption effects on movements. All the observed symptoms reduced when ascorbic acid was administered, and it diminished lethality in all cases. Ascorbic acid maintained nematodes’ postural capacities. The results suggest that nitrites’ nonspecific toxicity in C. elegans can be mitigated by ascorbic acid, as previously evidenced in other biological systems. Thus, our results reveal the ability of C. elegans to reproduce the known protective effect of ascorbic acid against nitrite.

Toxic mechanism of pyrene to catalase and protective effects of vitamin C: Studies at the molecular and cell levels

Polycyclic aromatic hydrocarbons, distributing extensively in the soil, would potentially threaten the soil organisms (Eisenia fetida) by triggering oxidative stress. As a ubiquitous antioxidant enzyme, catalase can protect organisms from oxidative damage. To reveal the potential impact of polycyclic aromatic hydrocarbon pyrene (Pyr) on catalase (CAT) and the possible protective effect of Ascorbic acid (vitamin C), multi-spectral and molecular docking techniques were used to investigate the influence of structure and function of catalase by pyrene. Fluorescence and circular dichroism analysis showed that pyrene would induce the microenvironmental changes of CAT amino acid residues and increase the α-helix in the secondary structure. Molecular simulation results indicated that the main binding force of pyrene around the active center of CAT is hydrogen bonding force. Furthermore, pyrene inhibited catalase activity to 69.9% compared with the blank group, but the degree of inhibition was significantly weakened after vitamin C added into the research group. Cell level experiments showed that pyrene can increase the level of ROS in the body cavity cell of earthworms, and put the cells under the threat of potential oxidative damage. Antioxidants-vitamin C has a protective effect on catalase and maintains the stability of intracellular ROS levels to a certain extent.

Protective effect of ascorbic acid against fenvalerate induced toxicity in air-breathing fish Clarias batrachus

The food demand in recent times has increased many folds. In order to augment the need for food, the agriculture practice is extensively carried out by the farmers and pesticides are widely used by them for the better yield of crops. Fishes are also cultivated by these farmers, and humans are consuming the fishes as they are very high nutritious food product. But, these pesticides through agricultural runoffs are contaminating the ponds as well the aquatic fauna like fish. The present research work deals with the evaluation of the protective effect of ascorbic acid on fenvalerate induced nephrotoxicity in Clarias batrachus. The pyrethroid pesticide- Fenvalerate EC 20% was administered directly in the water contained in the aquarium at the dose of 0.027 ppm, 0.042 ppm and 0.083 ppm respectively for 96 hrs hours after the dose calculation through LC50. Thereafter, ascorbic acid was administered orally by gastric intubation method at the dose of 200 mg/Kg body weight per day for 04 days to each pesticide treated group. The study revealed that, after the exposure of fenvalerate, there was significant damage at the biochemical levels like urea, creatinine, protein and albumin and histopathological study of kidney tissue in fish C. batrachus. But, after the administration of ascorbic acid, there was a significant restoration in the biochemical levels and in histopathology of the kidney of fish. The study concluded that Ascorbic acid possessed protective effect against fenvalerate induced toxicity in C. batrachus.

Pyrethroid-Induced Organ Toxicity and Anti-Oxidant-Supplemented Amelioration of Toxicity and Organ Damage: The Protective Roles of Ascorbic Acid and α-Tocopherol.

The pyrethroid toxicants, fatal at high doses, are found as remnants of crop pesticides and ingredients of commercially available insecticides. The toxic effects of high-content insecticidal pyrethroid formulations are available in 0.05 g, 1.17 g, and 0.04 g pyrethroid-instilled products, namely burning coils, pyrethroid-soaked mats, and liquid formulations of pyrethroids that release pyrethroid vapor/smoke upon heating. They provided 5.46 g/kg, 21.15 g/kg, and 4.24 g/kg of toxicants to the experimental animals over a total of 3 weeks/5 h per os (p.o.) administration, producing necrosis, hyperemia, and fatty changes in the liver; fiber separation in cardiac muscles; atrophy, lymphatic infiltration, blood vessel congestion, and hyperemia in the heart tissues of the experimental animals. The glomerular tuft necrosis, cytoplasmic degeneration of renal tubular cells, necrotic tubules, congestion, and dilatation of blood vessels were observed in the kidney tissue of intoxicated animals. Air-space enlargement, interstitial inflammation, lymphocyte infiltration aggregates, connective tissue infiltration by inflammatory cells, and hyperemia were found in the lung tissues. The pyrethroid toxicants also produced nervous tissue degeneration and decreased neurons in the brain, which were observed through histopathological examinations of the brain, lungs, heart, kidneys, and liver. The protective effects of ascorbic acid (AA/vitamin C) and α-tocopherol (E307/vitamin E) at 100 mg/kg oral doses administered daily for the entire period of the toxicant exposure of three weeks to the experimental mice, aged between 3–4 months and weighing ≈30 g, ameliorated the tissue damage, as observed through the histopathological examinations. The ascorbic acid caused recovery of the liver, kidney, brain, and heart tissue damage, while α-tocopherol was effective at ameliorating the damage in the kidneys and lung tissue compared with the control groups. The high levels of tissue damage recovery suggested a prophylactic effect of the concurrent use of ascorbic acid and α-tocopherol for the subjects under the exposure of pyrethroids.

The Protective Effect of Ascorbic Acid and Curcumin on the Chronic Toxicity of Meloxicam on the Testis of Adult Albino Rats

Meloxicam is a type of NSAIDs that has more selectivity on COX-2. Rehashed organization of meloxicam was accounted for to instigate testicular poisonousness, while curcumin and ascorbic corrosive have defensive properties against testicular injury. This examination was expected to explore the poisonous impacts of constant meloxicam organization on the testis, assess the part of oxidative worry in this impact and assess the conceivable defensive impact of curcumin and nutrient C each alone on this harmfulness. For progressive 63 days, grown-up male pale skinned person rodents were designated into 7 gatherings. Gathering A, regulated refined water; bunch B, directed corn oil; bunch C, managed curcumin [100 mg/kg/day intragastric] broke down in corn oil; bunch D, administrated ascorbic corrosive [200 mg/kg/day intragastric] disintegrated in refined water; bunch E, administrated meloxicam [8 mg/kg/day intragastric] broke down in refined water; bunch F, administrated intragastric meloxicam and curcumin in similar past portions and gathering G, administrated intragastric meloxicam and ascorbic corrosive in similar past dosages. Blood and testis tissue tests were gathered for biochemical, histopathological, and ultrastructural assessment. The outcomes uncovered that meloxicam organization in high rehashed dosages prompted a critical lessening in testis weight, sperm boundaries, and cell reinforcement movement of testicular tissue. Plasma testosterone level demonstrated non-critical lessening. Histopathological assessment uncovered rounded degeneration, intercellular vaculaization, interstitial edema and blockage of veins. The ultrastructure assessment uncovered cytoplasmic vacuolations and mitochondrial growing of spermatogenic and sertoli cells. Attendant organization of curcumin or ascorbic corrosive with meloxicam improved these changes. End: The outcomes explained the solid defensive impact of curcumin and ascorbic acids each alone on meloxicam prompted testicular harmfulness in rodents at biochemical, histopathological, and ultrastructural levels.

In Vitro Protective Effect of Ascorbic Acid Against Antibiotic-Induced Hepatotoxicity.

Although antibiotic-induced hepatotoxicity is recoverable with mild impairment, and some cases were reported to cause morbidity. However, an adjuvant is essential in reducing such incidences. The aim of this study is to evaluate the protective effect of ascorbic acid on antibiotic induced liver toxicity using liver slices. Fresh liver slices were incubated with different concentrations of sulfamethoxazole tetracycline and clavulanic acid along with ascorbic acid (200μg/ml) for 2 hours. The liver homogenate was assessed for markers like ALT, AST, MDA and CAT levels. Cytotoxicity assessment was performed using MTT assay. Incubating liver slices with all three antibiotics shows elevated levels of aminotransferases, MDA and CAT enzyme when compared to the control groups which indicates the level of hepatotoxicity. In the presence of ascorbic acid, the elevated levels of TBARS, ALT and AST were significantly reduced which showcases the protective effect of ascorbic acid. The percentage survival of cell was also shown to have improved while accessed using cell viability assay. Obtained data suggests that consuming vitamin C or vitamin C containing food like citrus fruits or green leafy vegetables equivalent to 3g/day during antibiotic treatment, perhaps put down the risk of liver toxicity to a greater extent.