Protective Role Of Ascorbic Acid Research Articles

Status of antioxidant defense system in chromium-induced Swiss mice tissues

Based on epidemiological studies, chromium(VI) compounds are considered as more toxic and carcinogenic than chromium(III) compounds. The deleterious effects of chromium(VI) compounds are diversified affecting almost all the organ systems in a wide variety of animals. The present study, describes the cytotoxic effects of chromium trioxide, a well-known chromium(VI) compound in three tissues (liver, kidney, lungs) of male Swiss mice during post-treatment phase (5th–8th week after treatment). Lipid peroxidation, an index of oxidative stress, was determined as thiobarbituric acid-reactive substances (TBA-Rs) in mice tissues dosed with a single intraperitoneal injection of chromium trioxide (1 mg/kg body weight). Tissue specific and statistically significant increases in TBA-Rs was observed in chromium-treated mice groups compared to controls in all the weeks of post-treatment. Endogenous ascorbic acid (vit-C) content of tissues which happens to be one of the stable antioxidants, declined significantly due to chromium-induction. Activity of antioxidative enzymes like superoxide dismutase (SOD), catalase (CT) and peroxidase (PD) was significantly inhibited among chromium-injected mice groups compared to respective controls. Protective role of ascorbic acid and the antioxidative enzymes in chromium-induced cytotoxicity in mice is discussed.

Aluminium-induced changes in hemato-biochemical parameters, lipid peroxidation and enzyme activities of male rabbits: protective role of ascorbic acid.

For a long time, aluminium (Al) has been considered an indifferent element from a toxicological point of view. In recent years, however, Al has been implicated in the pathogenesis of several clinical disorders, such as dialysis dementia, the fulminant neurological disorder that can develop in patients on renal dialysis. Therefore, the present experiment was carried out to determine the effectiveness of l-ascorbic acid (AA) in alleviating the toxicity of aluminium chloride (AlCl3) on certain hemato-biochemical parameters, lipid peroxidation and enzyme activities of male New Zealand white rabbits. Six rabbits per group were assigned to 1 of 4 treatment groups: 0mg AA and 0mg AlCl3/kg body weight (BW) (control); 40 mg AA/kg BW; 34 mg AlCl3/kg BW (1/25 LD50); 34 mg AlCl3 plus 40 mg AA/kg BW. Rabbits were orally administered their respective doses every other day for 16 weeks. Evaluations were made for lipid peroxidation, enzyme activities and hemato-biochemical parameters. Results obtained showed that AlCl3 significantly (P<0.05) induced free radicals and decreased the activity of glutathione S-transferase (GST) and the levels of sulfhydryl groups (SH groups) in rabbit plasma, liver, brain, testes and kidney. Aspartate aminotransferase (AST), alanine aminotransferase (ALT), alkaline phosphatase (AlP), acid phosphatase (AcP), and phosphorylase activities were significantly decreased in liver and testes due to AlCl3 administration. While, plasma, liver, testes and brain lactate dehydrogenase (LDH) activities were significantly increased. Contrariwise, the activity of acetylcholinesterase (AChE) was significantly decreased in brain and plasma. Aluminium treatment caused a significant decrease in plasma total lipids (TL), blood haemoglobin (Hb), total erythrocytic count (TEC) and packed cell volume (PCV), and increased total leukocyte count (TLC) and the concentrations of glucose, urea, creatinine, bilirubin and cholesterol. Ascorbic acid alone significantly decreased the levels of free radicals, TL, cholesterol, glucose and creatinine, and increased the activity of GST, SH groups, Hb, TEC and PCV. While, the rest of the tested parameters were not affected. Also, the present study showed that ascorbic acid can be effective in the protection of aluminium-induced toxicity.

Protective role of ascorbic acid against lead toxicity in blood of albino mice as revealed by metal uptake, lipid profiles, and ultrastructural features of erythrocytes.

Protective role of ascorbic acid against lead toxicity in blood of albino mice as revealed by metal uptake, lipid profiles, and ultrastructural features of erythrocytes.

Microdialysis Measurement of Ascorbic Acid in Rabbit Vitreous after Photodynamic Reaction

A method for long-term intravitreous microdialysis was used to measure endogenous reduced ascorbic acid in the vitreous of rabbits by HPLC-ECD before and after exposure to intense visible light in the presence of fluorescein. Cellulose microdialysis probes were implanted into the vitreous humor of each eye and after stabilization ascorbic acid measurements were recorded over a 14 day period. Under this experimental condition, normal ascorbic acid concentrations in vitreous varied from 98.0±9.8 to 106.9±20.3μM(mean±S.D.). The eyes received light irradiation (25000lux) for 2hr and fluorescein was used as the photosensitizer once or twice. No immediate effects on ascorbic acid concentrations could be observed in the eyes irradiated twice without fluorescein i.v. injections and in the twice fluorescein injected without irradiation. However, in the eyes irradiated once with fluorescein (30mgkg−1), ascorbic acid concentration after irradiation significantly decreased from day 2 and continued over a period of 10 days compared with that before irradiation and maximal reduction was 32.6% (P<0.005) on day 6 after irradiation. By day 13, the ascorbic acid concentration returned to control levels (P>0.01). In the eyes irradiated twice with fluorescein injections, ascorbic acid concentration after irradiation decreased even more over the experimental period and the maximal reduction was 65.5% (P<0.005) on day 5 after irradiation and did not recover over the next 9 days. In the eyes irradiated twice with fluorescein injections plus administration of ascorbic acid (150mgkg−1) 30min before irradiation, a significant increase (52.5%) of ascorbic acid (P<0.005) was found on day 1 and control levels of ascorbic acid were maintained from day 2 onward. The protective role of ascorbic acid in the vitreous humor against photodynamic reaction is suggested.

Protective role of ascorbic acid to enhance semen quality of rabbits treated with sublethal doses of aflatoxin B 1

Aflatoxins are toxic to a wide variety of animals, including man. The antioxidant ascorbic acid (AA) plays an important role in various physiological processes in the body including detoxification of different toxic compounds. The objective of this study was to evaluate the effects of AA on productive and reproductive characteristics of mature male rabbits given two sublethal doses (15 or 30 μg/kg of body weight; every other day) of aflatoxin B 1 (AFB 1). The experiment lasted 18 weeks and included two periods: a treatment period (first 9 weeks) where the animals were given the tested materials, and a recovery period (second 9 weeks) where all the drugs were withdrawn. Results showed that live body weight (LBW), dry matter intake (DMI), relative testes weight (RTW), and serum testosterone were significantly reduced ( P<0.05) by treatment with AFB 1 in a dose-dependent manner, and these effects continued during the recovery period. Aflatoxin treatment also decreased ( P<0.05) ejaculate volume, sperm concentration, total sperm output, sperm motility index, and semen initial fructose concentration. The negative effects of aflatoxin on semen characteristics were dose-dependent and continued during the recovery period. Treatment with AA increased ( P<0.05) LBW, DMI, RTW, serum testosterone concentration, improved semen characteristics, and alleviated the negative effects of AFB 1. Aflatoxin treatment increased ( P<0.05) the numbers of abnormal and dead sperms in a dose-dependent manner, and this effect continued during the recovery period. Treatment with AA alleviated the negative effects of AFB1 during treatment and recovery periods. Results demonstrated the beneficial influences of AA in reducing the negative effects of AFB 1 on production and reproduction of male rabbits.

Protective role of ascorbic acid against damage to male germ cells in rainbow trout (Oncorhynchus mykiss)

Low antioxidant levels have been implicated in damage to sperm DNA. We used a teleost fish to test if low paternal vitamin C status may cause mutations to the sperm and birth defects. During spermatogenesis, rainbow trout (Oncorhynchus mykiss) males were fed diets with graded levels of ascorbic acid derivative that were below and severalfold higher than those required for maximum growth. This treatment resulted in corresponding changes in levels of vitamin C in seminal plasma. We found that low levels of vitamin C in seminal plasma of rainbow trout were associated with a high percentage of abnormal embryos in the offspring. Among abnormal embryos, 34.8% were haploids or aneuploids, as revealed by flow cytometric measurement of DNA content. We found that UV-irradiated sperm gave rise to progeny with abnormalities similar to those resulting from sperm with low levels of antioxidants in seminal plasma. Ascorbic acid applied directly to semen did not prevent damage due to UV irradiation. These results provide the first experimental evidence that the lack or low levels of ascorbic acid in semen correlate with damage to male germ cells.

Protective role of ascorbic acid against damage to male germ cells in rainbow trout (&lt;i&gt;Oncorhynchus mykiss&lt;/i&gt;)

Protective role of ascorbic acid against damage to male germ cells in rainbow trout (&lt;i&gt;Oncorhynchus mykiss&lt;/i&gt;)

Vitamin C mediated protection on cisplatin induced mutagenicity in mice

In present studies the development of chromosomal aberrations, micronuclei in bone marrow cells and sperm head abnormalities were used as mutagenic bioassay in Swiss albino mice treated with cisplatin alone or ascorbic plus cisplatin. It was noted that in the combined treated hosts the frequency of all the mutagenic parameters were always significantly less than that treated with cisplatin alone. These findings suggest a protective role of ascorbic acid against cisplatin induced mutagenic potentials. Interestingly, in combined treated hosts glutathione (GSH) level in bone marrow cells increased significantly which may suggest a possible mechanism of ascorbic acid mediated protection against cisplatin induced mutagenic potentials in the hosts.

Effects of season and dietary ascorbic acid on some biochemical characteristics of rainbow trout (Oncorhynchus mykiss) semen

During the reproductive season, rainbow trout spermatozoa are stored in the sperm ducts for several months. There is no sperm production at this time since spermatogenesis is completed before spawning. To leam more about characteristics of semen during such a long storage, we analyzed changes in protein concentrations, anti-proteinase activity in seminal plasma and sperm aspartate aminotransferase activity during an extended reproductive period during which fish were fed diets supplemented with various ascorbic acid concentrations. Seminal plasma protein concentration and anti-proteinase activity declined toward the end of the reproductive season. These phenomena may be related to oncoming proteolytic events leading to degradation of the sperm. Protein concentrations and anti-proteinase activities were strongly correlated within groups of different ascorbic acid supplementations and several sampling dates (r=0.6-0.9 in most cases, p<0.05). Ascorbic acid deficiency resulted in a decrease in both parameter levels as compared to levels in groups with vitamin C supplement (p<0.08). Deficiency also resulted in lower stimulation of aspartate aminotransferase by an exogenous pyridoxal 5'-phosphate in comparison to fish fed vitamin C-supplemented diets (p<0.05). These results support earlier studies suggesting a protective role of ascorbic acid toward maintaining sperm quality.

Effect of ascorbic acid in the detoxification of the insecticide dimethoate in the bone marrow erythrocytes of mice

The antimutagenic potential of ascorbic acid in the detoxification of the organophosphorus insecticide dimethoate was evaluated in female Swiss albino mice using the in vivo bone marrow micronucleus test. Groups of three mice were treated with distilled water (control), 1% dimethyl sulphoxide (solvent control), or 86, 129.5 or 259 mg ascorbic acid/kg body weight, with or without the concurrent administration of 150 mg dimethoate/kg. There was a statistically significant increase in the frequency of micronuclei in dimethoate-treated mice. However, in mice that were given dimethoate and ascorbic acid simultaneously, the numbers of micronuclei did not differ significantly from control values, thus indicating the protective role of ascorbic acid.

Protective role of ascorbic acid against lipid peroxidation and myocardial injury.

Ascorbic acid (AH2) is a potential scavenger of superoxide radical and singlet oxygen. In the guinea pig, marginal AH2 deficiency results in intracellular oxidative damage in the cardiac tissue as evidenced by lipid peroxidation, formation of fluorescent pigment and loss of structural integrity of the microsomal membranes. The oxidative damage does not occur due to lack of enzymatic scavengers of reactive oxygen species such as superoxide dismutase, catalase and glutathione peroxidase. Also, glutathione transferase activity is not decreased in AH2 deficiency. Lipid peroxidation, fluorescent pigment formation and protein modification disappear after AH2 therapy. These results, if extra-polated to human beings, would indicate that chronic subclinical AH2 deficiency may result in progressive oxidative damage which in the long run may lead to permanent degenerative diseases in the heart.

Dietary Vitamin C Intake and Concentrations in the Body Fluids and Cells of Male Smokers and Nonsmokers

Inhaled cigarette smoke releases a variety of oxidizing agents. Ascorbic acid is recognized as an important biological antioxidant. To better characterize the antioxidant protective role of ascorbic acid, a comparison of ascorbic acid concentrations in plasma, leukocytes, bronchoalveolar lavage fluid and alveolar macrophages from a homogeneous group of healthy male smokers (n = 10) and nonsmokers (n = 14) was investigated. The resulting ascorbic acid contents were (means ± SD) 91 ± 25 (n = 10) and 87 ± 25 (n = 14) μmol/L in plasma, 2.09 ± 0.62 (n = 7) and 2.12 ± 0.77 (n = 11) μmol/109 cells in mononuclear leukocytes, 3.2 ± 2.2 (n = 10) and 1.7 ± 1.5 (n = 13) μmol/L in bronchoalveolar lavage fluid and 3.4 ± 2.3 (n = 8) and 1.6 ± 1.3 (n = 6) μmol/109 cells in alveolar macrophages from smokers and nonsmokers, respectively. Mean daily dietary vitamin C intake was 116 ± 68 and 107 ± 59 mg/d for smokers and nonsmokers, respectively. The ascorbic acid contents of bronchoalveolar lavage [3.9 ± 1.9 μmol/L (n = 8)] and alveolar macrophages [4.1 ± 2.1 μmol/109 cells (n = 6)] of smokers consuming 15 to 20 cigarettes/d were significantly higher (P < 0.05) than those of nonsmokers. The increased content of ascorbic acid in bronchoalveolar lavage and in alveolar macrophages of smokers compared with nonsmokers may reflect a defensive mechanism against free radical species derived from cigarette smoke.

Bio-elimination and organ retention profile of benzanthrone in scorbutic and non-scorbutic guinea pigs

The retention and bio-elimination of benzanthrone (BA) in scorbutic and non-scorbutic guinea pigs was investigated to understand the protective role of ascorbic acid. Oral intubation of 14C-BA to scorbutic and non-scorbutic guinea pigs showed a total recovery of around 91% radioactivity through urine, faeces and tissues. Recovery of radiolabelled BA through urine (28%) and faeces (22%) up to 96 hrs averaged 50%, whereas residual radioactivity in liver and testis experienced a recovery of 29% in scorbutic animals. In non-scorbutic animals there was an increased recovery of radioactivity through urine (37%) and faeces (31%) with a decrease in retention (10%) in liver and testis. These results suggest that ascorbic acid facilitates the mobilization and bio-elimination of BA and thereby can decrease the toxicity of the compound.

Protective Role of Ascorbic Acid Against Asbestos Induced Toxicity in Rat Lung: In Vitro Study

Asbestos fibers adsorb cytochrome P-450 and P-448 proteins from rat lung micosomal fractions and liberate heme from cytochrome P-448 on prolonged incubation in vitro. further, fibers, decrease the activities of benzo(a)pyrene hydroxylase and glutathione-S-transferase in microsomal and cytosolic fractions respectively. Mineral fibers also stimulate both the enzymatic (NADPH-induced) and non-enzymatic (Fe2(+)-induced) lipid peroxidation in microsomal fractions. Preincubation of microsomal and cytosolic fractions with a physiological concentration of ascorbic acid ameliorates, to a large extent, the changes induced by asbestos fibers.

Effect of Photic Injury on the Retinal Tissues

In order to study the tissue damages in photic injury of the retina, the macula and posterior pole of the rhesus monkey were exposed to the light of an indirect ophthalmoscope. During the acute phase of the injury, disruption of the blood-retinal barrier appeared to be an early and sensitive indicator of retinal pigment epithelial damage and cyclic-GMP-phosphodiesterase of the photoreceptor lamella was inactivated. These lesions were followed for 2 to 5 years. Focal chronic decompensation of the blood-retinal barrier and subretinal pigment epithelial neovascularization were noted in the chronic degenerative phase of this photic maculopathy. A possible protective role of ascorbic acid in mild photic injury was proposed.

Protective role of ascorbic acid in fishes exposed to organochlorine pollution.

Protective role of ascorbic acid on the toxic effect of aldrin pollution in an air-breathing fish Channa punctatus Bloch is reported. Fishes fed with aldrin mixed diet at 0.25% showed 25% mortality in 30 days. Mortality is preceded by certain changes in peripheral blood such as polycythemia and leucocytosis with increased thrombocyte but decreased neutrophil population. However, a massive dose of ascorbic acid (500 mg/100 g diet) was found to considerably neutralize the toxic effect as evidenced by 10-fold decrease in mortality and significantly lowered haematological response. The significance of these studies in the light of physiological role of ascorbic acid as a micronutrient for protection against pollution stress is discussed.