Impact of massive ascorbic acid supplementation on alcohol induced oxidative stress in guinea pigs
Department of Biochemistry, University of Kerala, Trivandrum, India. Toxicology Letters
(Impact Factor: 3.26).
03/1999; 104(3):221-9. DOI: 10.1016/S0378-4274(98)00377-4
The effects of a mega dose of ascorbic acid (AA) on alcohol induced peroxidative damages were investigated in guinea pigs. In the present study, four groups of male guinea pigs were maintained for 30 days as follows. (1) Control group (1 mg AA/100 g body wt); (2) Ethanol group (1 mg AA/100 g body wt. + 9 g ethanol/kg body wt); (3) AA group (25 mg AA/100 g body wt); (4) AA + ethanol group (25 mg AA/100 g body wt. + 9 g ethanol/kg). Results revealed that alcohol induced significant lipid peroxidation, since the lipid peroxidation products malondialdehyde (MDA), hydroperoxides and conjugated dienes were elevated. The activities of scavenging enzymes superoxide dismutase (SOD), catalase were reduced. However, supplementation of AA along with alcohol reduced the lipid peroxidation products in the liver and enhanced the activities of scavenging enzymes. Activities of glutathione peroxidase and reductase were also greater in guinea pigs given alcohol + AA in comparison with those given alcohol alone. Administration of ascorbic acid also reduced the activity of gamma-glutamyl transpeptidase (GGT), the marker enzyme of alcohol induced toxicity. The vitamin E level, which was reduced by alcohol intake, was raised by the co-administration of AA and alcohol. These studies suggest that a mega dose of AA helps in the prevention of alcohol induced oxidative stress by enhancing the antioxidant capacity and also by reducing the lipid peroxidation products.
Available from: onlinelibrary.wiley.com
- "To preserve the healthy heart from various challenges, including oxidative stress, the therapeutic usage of antioxidants and reducing agents, including Vitamin E, Vitamin C and free radical scavengers (Helen et al., 2000; Suresh et al., 1999) has been trialed. In order to overcome the limited advantages of the use of a single antioxidant, many researchers are interested in antioxidant-based composite therapy for the prevention and repair of complex myocardial diseases, which are related to oxidative stress. "
[Show abstract] [Hide abstract]
ABSTRACT: The water extract of Omija (Omija) has been used traditionally in the treatment of ischemic damage of the heart and brain tissues. However, little is known about the mechanism by which it rescues myocardial cells from oxidative stress. This study was designed to investigate the protective mechanisms of Omija on H(2)O(2)-induced cytotoxicity in H9c2 cardiomyoblast cells. Treatment with H(2)O(2) resulted in the death of H9c2 cells, characterized by apparent apoptotic features, including fragmentation of the nucleus and an increase in the sub-G(0)/G(1) fraction of the cell cycle. However, Omija markedly suppressed the apoptotic characteristics of H9c2 cells induced by H(2)O(2). In addition, Omija suppressed the features of mitochondrial dysfunction, including changes in the mitochondrial membrane potential and cytosolic release of cytochrome c in H(2)O(2)-treated cells. Treatment with Omija further inhibited the catalytic activation of caspase-9 and caspase-3 and induction of Fas by H(2)O(2). Taken together, these data indicate that the water extract of Omija protects H9c2 cardiomyoblast cells from oxidative stress of H(2)O(2) through inhibition of mitochondrial dysfunction and activation of intrinsic caspase cascades, including caspase-3 and caspase-9.
[Show abstract] [Hide abstract]
ABSTRACT: The aim of this study was to investigate what kind of stress vitamin C could alleviate. Experiments were performed using male
ICR mice. Vitamin C (1, 5, 25, and 100 mg/kg) was administered orally daily for 7 days without stress and then were given
for 5 days with electroshock (ES) or restraint stress (RS). After loading final stress, we recorded stress-related behaviors
and measured the levels of blood corticosterone. Vitamin C supplementation (25 and 100 mg/kg) partially blocked stress-related
behaviors such as freezing, smelling, burrowing, facewashing, and grooming. It decreased also staying time in closed arms.
Stress responses induced by ES but not immobility were also significantly alleviated by vitamin C. Vitamin C (25 and 100 mg/kg)
decreased corticosterone level increased by ES. Swimming time in cold water (8±2°C) was not changed by vitamin C, but crossing
frequency in the electric field was increased by vitamin C (25 mg/kg). These results suggest that vitamin C supplementation
can prevent damages or diseases induced by stress, especially psychological stress.
Keywordsvitamin C-electro-shock stress-restraint stress-behavior-corticosterone
[Show abstract] [Hide abstract]
ABSTRACT: Protective effects of Yijin-tang extract (YTE) were investigated on ethanol-induced acute gastric injury. Simultaneous determination of six components, homogentisic aicd, liquiritin, hesperidin, neohesperidin, poncirin, and glycyrrhizin was performed in YTE by high performance liquid chromatography-photodiode. Acute gastric lesion was induced by oral administration of absolute ethanol (5 mL/kg). The positive control (omeprazole, 50 mg/kg) and YTE groups (200 and 400 mg/kg) were administered by oral gavage 2 h prior to ethanol treatment. The animals were sacrificed 1 h after receiving ethanol treatment. Acute toxicity study was performed to evaluate the safety of YTE. YTE protected gastric mucosa against ethanol-induced acute gastric injury including hemorrhage and hyperemia. YTE reduced the elevated lipid peroxidation of stomach and increased the activities of antioxidant enzyme. In the acute toxicity study, YTE did not cause any toxic effect at the dose level of 2000 mg/kg in rats. These results showed that YTE protects gastric mucosa from ethanolinduced acute gastric injury via increasing the antioxidant status. We suggest that YTE has a potential as a therapeutic agent for acute gastric injury.
Data provided are for informational purposes only. Although carefully collected, accuracy cannot be guaranteed. The impact factor represents a rough estimation of the journal's impact factor and does not reflect the actual current impact factor. Publisher conditions are provided by RoMEO. Differing provisions from the publisher's actual policy or licence agreement may be applicable.