Intraperitoneal Administration Of Vitamin Research Articles

Effect of intraperitoneal administration of vitamin C (ascorbic acid) on anemia in experimental Trypanosoma congolense infected rabbits

The effect of Vitamin C supplementation on anemia in experimental Trypanosoma congolense infected rabbits was investigated. Locally bred rabbits were infected with 6 ´ 106 trypanosomes per rabbit and infection was monitored for 5 weeks. Packed cell volume (PCV), Total leucocytes count (TLC) and parasite load were determined weekly. Vitamin C supplementation did not significantly affect parasitaemia in the first two weeks of infection but parasitaemia was significantly decreased (p < 0.01) in the last three weeks of infection. Anemia developed in theT. congolense infected rabbits as evidenced by reduced PCV during the course of the experiment. Treatment of infection with Vitamin C had slightly, though not to a significant extent ameliorated the T. congolense induced anemia. Leucocytosis was lower in the infected treated rabbits than in the infected untreated rabbits. It was concluded that Vitamin C did not prevent the anemia or the leucocytosis caused by T. congolense, but it slightly though not to a significant level ameliorated the condition. Key words: Tryponosoma congolense, vitamin C (Ascorbic acid), anemia.

Chronic vitamin C administration induces thermal hyperalgesia in male rats

Against a backdrop of neurological effects, the effects of acute and chronic administration of vitamin C (600mg/kg) on pain processing were investigated in male rats. Chronic administration of vitamin C induced significant thermal hyperalgesia while acute administration had no effect. In addition, the intraperitoneal administration of vitamin C produced observable abdominal writtings similar to what has been observed with acetic acid. We conclude that chronic vitamin C exerts facilitatory central nervous system effects and a possibility of using intraperitoneal injection of vitamin C as an animal model of pain is suggested. Keywords: vitamin C, pain, hyperalgesia, nociception, ascorbic acidNigerian Journal of Health and Biomedical Sciences Vol. 4(2) 2005: 153-155

Protective action of vitamins on the spermatogenesis in lead-treated Swiss mice

The protective action of vitamins C and E against lead acetate-induced reduced sperm count and sperm abnormalities in Swiss mice has been studied. Intraperitoneal injection of lead acetate (10 mg/kg body weight) in the present study stimulates lipid peroxidation in the testicular tissue, indicated by a significant increase in malondialdehyde content in the experimental mice group. This is associated with an increased generation of noxious reactive oxygen species (ROS). Significantly reduced sperm count associated with increased sperm abnormality percentage in the lead-injected mice group compared to controls substantially proves the ongoing damaging effects of lead-induced ROS on developing germ cells. However, intraperitoneal administration of vitamin C (Vit C) at a concentration equivalent to the human therapeutic dose (10 mg/kg body weight) was able to minimize significantly the testicular malondialdehyde content with a concomitant increase in sperm count and significant decrease in the percentage of abnormal sperm population. Vitamin E (Vit E) (100 mg/kg body weight) treatment of a batch of lead-injected mice had a similar effect as Vit C but with a comparatively lower efficacy. On the other hand, co-administration of both vitamins (Vit C+Vit E) at the above mentioned doses to lead-treated mice led to the most significant decline in malondialdehyde content along with elevated sperm count and reduction in the percentage of abnormal sperm population. The protective action and the synergistic action of both vitamins (C and E) against lead-induced genotoxicity are discussed.

Prevention of Peritoneal Adhesions by Intraperitoneal Administration of Vitamin E: An Experimental Study in Rats

Previous studies have shown dietary supplements of vitamin E to reduce the incidence of postoperative peritoneal adhesions. The objective of this study was to show the effect of intramuscular or intraperitoneal administration of vitamin E on peritoneal adhesions. Eighty rats were divided into four groups: Group A (control), Group B (intramuscular vitamin E), Group C (intraperitoneal olive oil, the vehicle/diluent of vitamin E), and Group D (intraperitoneal vitamin E diluted in olive oil). The same experimental method was used in all rats to produce adhesions, consisting of cecal abrasion and ligature of the adjacent parietal peritoneum. The rats were killed at 14 days to assess the adhesions occurring. The results were analyzed using a chi-squared test. All animals in Groups A, B, and C had substantial adhesions. In Group D, 11 rats had insubstantial adhesions and only 4 had substantial adhesions. There were no significant differences between Groups A, B, and C in terms of percent formation of adhesions. A significant difference was found between Group D (vitamin E plus olive oil by the intraperitoneal route) and each of the experimental groups, A, B, and C (P < 0.0005). Our results show that intraperitoneal administration of vitamin E just before closing the laparotomy was effective for reducing adhesion formation. By contrast, the same effect was not achieved after intramuscular administration.

Antinociceptive effect induced by intraperitoneal administration of vitamin K 2 (menatetrenone) in ICR mice

The antinociceptive effect of vitamin K 2 (menatetrenone) in mice was examined using tail-flick and formalin test. Menatetrenone at doses of 10, 50 and 100 mg/kg, i.p. produced a dose-dependent and significant inhibition of the tail-flick response in mice. Menatetrenone (50 and 100 mg/kg, i.p.) had no significant effect on the duration of the first phase of the formalin-induced flinching. However, menatetrenone (100 mg/kg, i.p.) significantly inhibited the second phase of the formalin-induced flinching. I.p. administration of menatetrenone (100 mg/kg) significantly reduced the duration of nociceptive responses induced by i.t. injection of bradykinin, but not of substance P, prostaglandin E 2 or N-methyl-D-aspartate (NMDA). These present data suggest that i.p. pretreatment with menatetrenone produced dose-dependent antinociceptive effect in mice. This effect may be, at least in part, mediated by the inhibition of bradykinin dependent nociceptive transmission in the spinal cord.

Effects of intraperitoneally-administered vitamin E and selenium on the blood biochemical and haematological parameters in rats.

The aim of this work was to determine the role of intraperitoneally-administered vitamin E and selenium on the biochemical and haematological parameters in the blood of rats. Thirty-two adult male Wistar rats were used in this study. All rats were randomly divided into four groups. The first group was used as the control. The second group was intraperitoneally administered with vitamin E (+/-(-)alpha-tocopheroryl acetate, 10 mg day-1), the third group with Se (Na2SeO3 0.2 mg over a day), and the fourth group with vitamin E and Se (vitamin E 10 mg + Na2SeO3 0.2 mg over a day). This administration was done for 5 weeks. Blood samples were taken from animals at the end of the dosage period and biochemical parameters in serum samples and haematological parameters in total blood were determined. The levels of total cholesterol (p < 0.01) and number of white blood cell (p < 0.001) in blood were significantly higher in the vitamin E group than in the control group. The levels of ALP, total cholesterol (p < 0.01) and number of white blood cells (p < 0.01) in blood were significantly higher in the selenium group than in the controls. The levels of glucose (p < 0.05), ALP (p < 0.01), total cholesterol (p < 0.001) and number of white blood cells (p < 0.01) were higher in the vitamin E and selenium combined group than in the controls. Other parameters considered within this trial (ALT, LDH, creatinine, albumin, total protein, amylase, creatine kinase, HDL triglycerides, total lipid, sodium, chloride, uric acids, red blood cell, haemoglobin, packed cell volume, MCV, MCH, MCHC) did not show statistically significant differences between the control and injected groups. The results indicated that blood glucose and total cholesterol levels, ALP activity and white blood cell counts were significantly increased by intraperitoneal administration of vitamin E and selenium in rats.

Aging and oxidative stress in neurodegeneration.

The effect of oxidative stress on the function of brain synapse, the difference in susceptibility of synapse to hyperoxia with age, and the changes in vitamin E status by stress and aging were investigated. Synaptic membrane permeability to sucrose was increased with age. When rats were subjected to hyperoxia, the membrane permeability on each age increased significantly. The susceptibility of synapse of 25 month old rats exposed to stress was about 2.5 times higher than unexposed old rats. The synaptic plasma membrane fluidity decreased significantly either in response to hyperoxia or during aging. The thiobarbituric acid reactive substances (TBARS) in the synaptic plasma membranes increased with age, and those in the membranes of oxygen-exposed rats were higher than in the unexposed rats. The cholesterol/phospholipids (C/P) ratio of the membranes increased significantly with age, and the values in the membranes of oxygen-exposed rats increased more significantly than in unexposed rats of each age. In a measurement of fatty acid content in the membranes, the content of docosahexaenoic acid (DHA, C22:6) decreased significantly during aging and by hyperoxia. These results suggest that free radicals derived from oxygen may attack nerve terminals and peroxidize the membrane, resulting in the deterioration of function of brain synapse, and that susceptibility of synapse to oxidative stress was significantly increased with age. Vitamin E content in the synaptic plasma membranes decreased with age. When rats were subjected to oxidative stress, the content was lower in each age than in normal rat membranes. An intraperitoneal administration of vitamin E prior to stress reduced these abnormalities. It is obvious that vitamin E contributes to the protection against nerve terminal dysfunction caused by oxidative stress.

Ascorbate-Fe2+ lipid-peroxidation of rat liver microsomes: effect of vitamin E and cytosolic proteins.

In the present study, we examined the effect of the intraperitoneal administration of vitamin E (100 mg/kg weight/24 h) on ascorbate (0.4 mM) induced lipid peroxidation of rat liver microsomes . We also analyzed the effect of hepatic cytosolic proteins on this process. The results indicate that the ascorbate induced light emission was 76% lower in microsomes (1 mg protein) obtained from vitamin E treated animals when compared with controls. In the presence of cytosolic protein (1 mg) the chemiluminescence of control microsomes diminished 55.8 and 59.5% when cytosol from controls and treated animals was used, respectively. The chemiluminescence of vitamin E microsomes diminished 25.03 and 22.08% when both types of cytosol were added to the medium. Dialyzed or treated at 70 degrees C cytosol was also able to inhibit the lipid peroxidation of either control or vitamin E rat liver microsomes. By means of gas chromatography we analyzed the fatty acid composition of native and peroxidated microsomes from both animal groups. The peroxidation affected principally arachidonic acid and its diminution was more evident in the control microsomes than in the microsomes from the vitamin E treated group. By HPLC we analyzed the vitamin E content in all subcellular fractions employed. In microsomes from the vitamin E-group, the content of vitamin was 11 times higher than in the control ones (0.678 +/- 0.1038 vs. 0.062 +/- 0.0045 microg alpha-tocopherol/mg protein, respectively), while levels in the cytosol from the vitamin E-group were only 2 times higher than in the control cytosol (0.057 +/- 0.0051 vs. 0.025 +/- 0.0015 microg alpha-tocopherol/mg protein, respectively).

Oxidative injury of synapse and alteration of antioxidative defense systems in rats, and its prevention by vitamin E.

In order to define whether active oxygen species actually induce oxidative damage to the nervous system, and how antioxidative defense systems are changed by oxidative stress, morphological and functional changes in the nervous system and antioxidant status were investigated. When rats were exposed to 100% oxygen in a chamber, many morphological changes, e.g. swollen astrocytes around vessels, deformed nuclei in nerve cells, pigmentation, swollen mitochondria, and abnormal accumulation of synaptic vesicles in swollen nerve terminals, were observed by electron microscopy. When synaptosomes isolated from oxygen-exposed rats were stimulated by KCl, acetylcholine release from the terminal was decreased more significantly than in synaptosomes from unexposed rats (P < 0.01). Synaptic plasma membrane fluidity decreased in response to oxygen exposure, and plasma membrane permeability to sucrose was increased significantly (P < 0.05). The cholesterol/phospholipid ratio of the plasma membranes was increased by oxidative stress and the content of unsaturated fatty acids, especially arachidonic acid and docosahexaenoic acid, decreased. The levels of thiobarbituric-acid-reactive substances in the plasma membranes of oxygen-exposed rats were significantly higher than in unexposed rats (P < 0.01). These results suggest that free radicals derived from oxygen may attack nerve terminals and peroxidize the plasma membrane. It was found that in response to the oxidative stress, the status of the defense system in synapse, i.e. the concentration of vitamin E, activities of superoxide dismutase and glutathione peroxidase changed, and that many of the changes observed were reduced remarkably by the intraperitoneal administration of vitamin E prior to stress. Data support the idea that vitamin E contributes to the protection against nerve dysfunction caused by oxidative stress.

Mammary Transfer of Vitamin E in Dairy Cows

Milk vitamin E from eight dairy cows was analyzed for vitamin E by HPLC during the 1st mo of lactation. Colostrum gave a mean value of 1.9μg α-tocopherol/ml while concentrations of fresh milk averaged .3μg α-tocopherol/ml. D-γ-tocopherol concentrations were observed in very small amounts. When six cows at the end of the 1st mo of lactation were injected intraperitoneally with an emulsion of dl-α-tocopherol acetate (5g), plasma and milk concentrations of α-tocopherol were increased from their original values of 4.5 μg/ml plasma and .3μg/ml fresh milk to 10.9μg/ml plasma and 1.6μg/ml fresh milk, 12h later. The results show that intraperitoneal administration of vitamin E to dairy cows in an effective way of increasing plasma and milk tocopherol concentration.

Vitamin A and tumor immunity.

Intraperitoneal administration of vitamin A into the BALB/c mice inoculated with a syngeneic fibrosarcoma, Meth A, caused a remarkable augmentation of tumor rejection. A cell-depletion technique revealed that the primary effector cells responsible for the augmented rejection were Thy-1 positive, Lyt-1 negative, Lyt-2 positive lymphocytes, suggesting the involvement of cytotoxic lymphocytes.

Liver and plasma lipids in vitamin E-deficient rats.

To investigate metabolic alterations during vitamin E-deficiency, the content of lipid peroxides and lipids in liver and plasma was determined using vitamin E-deficient rats, and its results were as follows : Lipid peroxide in the liver from vitamin E-deficient rats increased about 3 times over the control group, and the value returned to the normal level after intraperitoneal administration of vitamin E in a dose of 50mg/kg/day for 6 days, but that in plasma was almost constant. In vitamin E-deficiency, C16 : 1, C18 : 1, and C20 : 4 increased mainly in triglycerides (TG) in liver lipids. C18 : 2 decreased in the fractions of phospholipids but not in TG fraction. On the other hand, in plasma from vitamin E-deficient rats, C18 : 1 increased and C18 : 2 decreased in all the fractions of lipids. Decrease of C20 : 4 was found in phosphatidylethanolamine (PE) and phosphatidylcholine (PC) in plasma lipids. Free fatty acids of plasma in vitamin E-deficiency increased by approx. 76%, and TG content increased about 73% in the liver and 35% in the plasma. The total cholesterol content of the liver and plasma from vitamin E-deficient rats increased about 55 and 20%, respectively. The content of phospholipids in the liver and plasma showed little change in vitamin E-deficiency.