Comparative effect of palm vitamin E and ranitidine on the healing of ethanol-induced gastric lesions in rats

The effect of palm vitamin E on the healing of ethanol-induced gastric lesion was compared with ranitidine. Fifty-six male rats of Sprague-Dawley species (200-250 g of weight) were randomly divided into three groups (N = 14). Gastric mucosal injury was induced by orogastric tube administration of 0.5 ml 100% ethanol. Immediately after induction, Group I (k) rats was fed with a normal diet (control), group II (p) was fed palm vitamin E enriched diet (150 mg/kg food), Group III(r) was treated with ranitidine 30 mg/kg body weight intraperitoneally and Group IV (p + r) was fed with palm vitamin E and treated with ranitidine 30 mg/kg body weight intraperitoneally of the same dose. The rats were killed at the end of 1 week and 3 weeks of treatment or feeding. The rate of gastric healing was faster in palm vitamin E treated group compared to control and ranitidine treated groups as shown by a lower mean ulcer index. The effect was seen as early as the first week of treatment whereas ranitidine did not show any healing effect even after 3 weeks of therapy. Neither gastric acidity nor gastric mucus production are involved in gastroprotective effect of palm vitamin E. The most probable mechanism is via reducing lipid peroxidation process as shown by a significant decrease in gastric MDA.     

Protective Effects of Ginger against Aspirin-Induced Gastric Ulcers in Rats

We investigated the mechanism underlying the protective effects of ginger against gastric damage induced by aspirin in rats. Gastric mucosal lesions were produced by orally administering 200 mg/kg aspirin suspended in 1% carboxymethylcellulose solution to pyloric-ligated male Wistar rats. Ginger powder (200 mg/kg) markedly reduced the aspirin-induced gastric hemorrhagic ulcer area. The total acidity of gastric juice was not significantly influenced by aspirin or ginger. Ginger powder did not affect the aspirin-induced reduction in mucosal prostaglandin E₂ (PGE₂) content; however, it did ameliorate the aspirin-induced increases in mucosal activity of the inducible form of NO synthase (iNOS) and plasma tumor necrosis factor (TNF)-α and interleukin (IL)-1β levels. In the next experiment, high and low doses of 6-gingerol and 6-shogaol were used instead of ginger powder in the same experimental model to examine their roles in the anti-ulcer mechanism of ginger. Both 6-gingerol and 6-shogaol reduced aspirin induced ulcer formation, mucosal iNOS and plasma TNF-α and IL-1β levels. In conclusion, ginger powder prevents the aspirin induced gastric ulcer formation by reducing mucosal iNOS activity and the plasma levels of inflammatory cytokines but does not affect gastric juice or acid production or mucosal PGE₂ content. This protective effect of ginger powder against gastric ulcers may be attributable to both gingerol and shogaol.     

The effects of palm vitamin E on stress hormone levels and gastric lesions in stress-induced rats

Introduction

This study examines the effects of palm vitamin E (PVE) or α-tocopherol (α-TF) supplementation on adrenocorticotropin hormone (ACTH), corticosterone and gastric lesions in rats exposed to water-immersion restraint stress (WIRS).

Material and methods

Sixty male Sprague-Dawley rats (200-250 g) were divided into three groups. Group I: 20 rats as a control group were given a normal diet. Group II: 20 rats received oral supplementation of PVE at 60 mg/kg body weight. Group III: 20 rats received oral supplementation of α-TF at 60 mg/kg body weight. After the treatment period of 28 days, each group was further subdivided into two groups: 10 rats not exposed to stress, and the other 10 rats subjected to WIRS for 3.5 h. Blood samples were taken to measure the ACTH and corticosterone levels. The rats were then sacrificed and the stomach excised and opened along the greater curvature and examined for lesions.

Results

Rats exposed to WIRS had lesions in their stomach mucosa. Our findings showed that dietary supplementation of PVE or α-TF was able to reduce gastric lesions significantly in comparison to the stressed controls. The WIRS increased plasma ACTH and corticosterone significantly. Palm vitamin E and α-TF treatments reduced these parameters significantly compared to the stressed controls.

Conclusions

Supplementation with either PVE or α-TF reduces the formation of gastric lesions, probably by inhibiting the elevation of ACTH and corticosterone levels induced by stress.     

Tocotrienols-rich diet decreases advanced glycosylation end-products in non-diabetic rats and improves glycemic control in streptozotocin-induced diabetic rats

This study determined the effects of palm vitamin E (TRF) diet on the levels of blood glucose, glycated hemoglobin (gHb), serum advanced glycosylation end-products (AGE) and malondialdehyde (MDA) of diabetic Sprague-Dawley rats. The rats received either control (normal rat chow), TRF diet (normal chow fortified with TRF at 1 g/kg) or Vitamin C diet (vitamin E-deficient but contained vitamin C at 45 g/kg). The animals were maintained on the respective diet for 4 weeks, made diabetic with streptozotocin (STZ), then followed-up for a further 8 weeks. At week-4, mean serum AGE levels of rats given TRF diet (0.7 +/- 0.3 units/ml) were significantly lower than those of control or Vitamin C diet rats (p pounds 0.03). The levels increased after STZ and became comparable to the other groups. At week 12, blood glucose (20.9 +/- 6.9 mM) and gHb (10.0 +/- 1.6%) of rats on TRF diet remained significantly low compared to that of control or Vitamin C diet rats (p pounds 0.03). MDA however, was not affected and remained comparable between groups throughout the study. This study showed that TRF may be a useful antioxidant; effectively prevented increase in AGE in normal rats, and caused decrease in blood glucose and gHb in diabetic rats. Further studies are needed to elucidate the mechanisms of action of TRF.     

Comparative efficacy of chamomile against omeprazole in aspirin-induced gastric ulcer in rats

The aim of the study was to compare the efficacy of chamomile versus omeprazole in the treatment of aspirin-induced gastric ulcer in rats. Animals were randomly assigned into three groups A, B and C (n?=?10 each). Aspirin (200 mg/kg, intragastric (i.g.)) was administered for three consecutive days, and then, two animals from each group were euthanized and formed the aspirin-induced gastric ulcer control group. The remaining animals (n?=?8 in each group) were administered with the following treatments: normal saline 9 % (0/5 mL, i.g.) (group A), omeprazole (2.3 mg/kg, i.p.) (group B) or chamomile decoction (25 mL/kg, i.g.) (group C) daily for 2 weeks. Histological analysis of tissue harvested from rats in groups B and C showed no significant difference, since ulcers in both treatment groups were completely cured. The results of this study suggest that chamomile could be used for the treatment of nonsteroidal anti-inflammatory drug-induced ulcers as an inexpensive alternative to omeprazole.     

Vitamin E but not St. John's wort mitigates leukopenia caused by cancer chemotherapy in rats

Dietary supplements are used by most patients with cancer. As nutraceuticals can interact with many drugs, this study investigated the effect of herbal remedies and vitamins on the toxicity of representative cancer chemotherapeutic agents. Fisher 344 rats were fed a standard cereal-based diet or the same diet with additional vitamin E in low (50 mg/kg) or high (750 mg/kg) concentrations, or with added St. John's wort (400 mg/kg). The LD50 was determined after the administration of chemotherapy drugs. Neither low or high vitamin E supplements nor St. John's wort significantly changed the LD50 for doxorubicin, docetaxel, or cyclophosphamide. The nadir white blood cell (WBC) count was significantly higher (P = 0.004) after docetaxel in rats supplemented with low-dose vitamin E, but the drop in WBC count from initial to nadir levels (Nfall) was greater in rats fed a diet containing high vitamin E supplementation (P = 0.04). Similarly, the Nfall was greater in the standard and high vitamin E dietary groups than in the low vitamin E group after cyclophosphamide (P = 0.03). No effect of vitamin E or St. John's wort supplementation occurred on doxorubicin pharmacokinetics. Neither vitamin E nor St. John's wort had an important effect on the mitochondrial deoxyribonucleic acid (DNA) damage caused by either doxorubicin or docetaxel. These data suggest that the leucopenia caused by some chemotherapeutic agents can be modified by dietary supplementation with vitamin E, but the effect seems to be dose-dependent. St. John's wort had neither a beneficial nor a detrimental effect on chemotherapy-induced toxicity.     

Effects of captopril on factors affecting gastric mucosal integrity in aspirin-induced gastric lesions in Sprague-Dawley rats

Introduction

Captopril is an angiotensin-converting enzyme inhibitor, which is used as an antihypertensive agent and has shown antioxidant properties. This study aims at determining the effects of captopril on factors affecting gastric mucosal integrity in aspirin-induced gastric lesions.

Material and methods

Eighteen male Sprague-Dawley (200-250 g) rats that were given aspirin (40 mg/100 g body weight) were divided into three groups: the control, captopril (1 mg/100 g body weight daily) and ranitidine (2.5 mg/100 g body weight twice daily) groups. Ranitidine and captopril were given orally for 28 days. Rats in all groups were sacrificed and the parameters measured.

Results

Captopril reduced gastric acidity, and increased gastric glutathione (GSH) and prostaglandin E₂ (PGE₂) significantly in comparison to the control group. Captopril also reduced malondialdehyde (MDA) and gastric lesions insignificantly compared to the control group. Ranitidine healed the lesions significantly compared to the control group. There was no difference between ranitidine and captopril on the severity of lesions, gastric acidity, MDA and GSH. Captopril increased PGE₂ compared to ranitidine (p < 0.05).

Conclusions

Captopril has desirable effects on the factors affecting gastric mucosal integrity (acidity, PGE₂ and GSH) and is comparable to ranitidine in ulcer healing.     

Differential effect of vitamin K and vitamin D supplementation on bone mass in young rats fed normal or low calcium diet

The purpose of this study was to clarify the differential effect of vitamin K and vitamin D supplementation on bone mass in young rats fed a normal or low calcium diet. Ninety female Sprague-Dawley rats, 6 weeks of age, were randomized by stratified weight method into nine groups with 10 rats in each group: baseline control, and 0.5% (normal) or 0.1% (low) calcium diet, either alone, or with vitamin K (30 mg/100g, food intake), vitamin D (25 micro g/100 g, food intake), or vitamin K + vitamin D. After 10 weeks of feeding, bone histomorphometric analyses were performed on cortical bone of the tibial shaft and cancellous bone of the proximal tibia. Vitamin K supplementation increased the maturation-related cancellous bone gain and retarded the reduction in the maturation-related cortical bone gain in rats fed a low calcium diet, and increased the maturation-related cortical bone gain in rats fed a normal calcium diet. Vitamin D supplementation reduced the maturation-related cancellous bone gain, prevented the reduction in periosteal bone gain, and enhanced the enlargement of the marrow cavity, with no significant effect on the reduction in the maturation-related cortical bone gain in rats fed a low calcium diet, and increased the maturation- related cancellous and cortical bone gains with increased periosteal bone gain in rats fed a normal calcium diet. An additive effect of vitamin K and vitamin D on the maturation- related cortical bone gain was found in rats fed a normal calcium diet. This study shows the differential effects of vitamin K and vitamin D supplementation on cancellous and cortical bone mass in young rats fed a normal or low calcium diet, as well as the additive effect on cortical bone under calcium sufficient condition.     

Protective effect of γ‐tocopherol‐enriched diet on N‐methyl‐N‐nitrosourea‐induced epithelial dysplasia in rat ventral prostate

Despite recent advances in understanding the biological basis of prostate cancer (PCa), the management of this disease remains a challenge. Chemoprotective agents have been used to protect against or eradicate prostate malignancies. Here, we investigated the protective effect of γ‐tocopherol on N‐methyl‐N‐nitrosourea (MNU)‐induced epithelial dysplasia in the rat ventral prostate (VP). Thirty‐two male Wistar rats were divided into four groups (n = 8): control (CT): healthy control animals fed a standard diet; control+γ‐tocopherol (CT+γT): healthy control animals without intervention fed a γ‐tocopherol‐enriched diet (20 mg/kg); N‐methyl‐N‐nitrosourea (MNU): rats that received a single dose of MNU (30 mg/kg) plus testosterone propionate (100 mg/kg) and were fed a standard diet; and MNU+γ‐tocopherol (MNU+γT): rats that received the same treatment of MNU plus testosterone and were fed with a γ‐tocopherol‐enriched diet (20 mg/kg). After 4 months, the VPs were excised to evaluate morphology, cell proliferation and apoptosis, as well as cyclooxygenase‐2 (Cox‐2), glutathione‐S‐transferase‐pi (GST‐pi) and androgen receptor (AR) protein expression, and matrix metalloproteinase‐9 (MMP‐9) activity. An increase in the incidence of epithelial dysplasias, such as stratified epithelial hyperplasia and squamous metaplasia, in the MNU group was accompanied by augmented cell proliferation, GST‐pi and Cox‐2 immunoexpression and pro‐MMP‐9 activity. Stromal thickening and inflammatory foci were also observed. The administration of a γ‐tocopherol‐enriched diet significantly attenuated the adverse effects of MNU in the VP. The incidence of epithelial dysplasia decreased, along with the cell proliferation index, GST‐pi and Cox‐2 immunoexpression. The gelatinolytic activity of pro‐MMP‐9 returned to the levels observed for the CT group. These results suggest that γ‐tocopherol acts as a protective agent against MNU‐induced prostatic disorders in the rat ventral prostate.     

Relationship between dietary retinol and lipofuscin in the retinal pigment epithelium

A variety of evidence suggests that autoxidation of cellular components probably plays a significant role in the age-related accumulation of lipofuscin, or age-pigment, in the mammalian retinal pigment epithelium (RPE). Among the likely candidates for conversion into RPE lipofuscin fluorophores via autoxidative mechanisms are vitamin A compounds, which are present in the retina and RPE in high concentrations. Vitamin E, an important lipid antioxidant, is likely to inhibit vitamin A autoxidation. Experiments were conducted to evaluate the significance of vitamin A autoxidation in the deposition of lipofuscin in the RPE. Albino rats were fed diets either supplemented with or lacking vitamin E. Each of these two groups of animals was further subdivided into three groups which were fed different levels of vitamin A palmitate: none, 14.0 mumol/kg diet, and 80.5 mumol/kg diet. After 26 weeks, the animals were killed and the RPE lipofuscin contents were determined by both fluorescence measurements and quantitative ultrastructural morphometry. Vitamin A palmitate deficiency led to significant reductions in RPE lipofuscin deposition, relative to the amounts of this pigment present in the groups receiving vitamin A palmitate in their diets. The relative magnitude of the vitamin A effect was greater in the vitamin E-supplemented groups than in the groups fed the diets deficient in vitamin E. This finding suggests that vitamin E interacts with vitamin A ester metabolites in vivo in a more complex manner than simply acting as an antioxidant protectant. Rats fed the diets containing the higher level of vitamin A palmitate failed to display elevated RPE lipofuscin contents relative to those in the rats fed 14.0 mumol of vitamin A palmitate/kg diet. Failure of high vitamin A intake to enhance RPE lipofuscin deposition may have been due to the fact that intake of vitamin A above normal levels did not lead to an elevation in vitamin A content of the retinal tissue. Establishing an effect of vitamin A deficiency on RPE lipofuscin deposition and characterization of the interactions between vitamins E and A are important steps toward defining precisely the molecular and cellular mechanisms underlying age-pigment accumulation in the RPE.     

Effect of partially refined palm oil in lipid profile in rats

Palm oil is rich in carotenoids, tocopherols and tocotrienols. This oil is refined for its human consumption bringing as a consequence an alteration of their properties. The objective of this study was to evaluate the effect of the partially refined, bleached and deodorized palm oil (RBD red) on the lipid profile and levels of vitamin A (retinol) and E (alpha tocopherol) in 4 groups of rats: B (commercial food Protinal for laboratory animals: ST + 5% egg yolk powder); C (ST + 5% egg yolk powder + 14 RBD red) both groups with induced hyperlipidemia; and D (ST + 14% RBD red), as compared with a control A (ST) during 35 days. The results were: the RBD red induced significative decreases of TC (total cholesterol) in groups C and D (81 +/- 11 mg/dL and 77 + 7 mg/dL), respectively, when compared with the control group (99 +/- 11 mg/dL) for 35 days experimentation. Additionally, an increment of the HDL-C (53 +/- 4 mg/dL) in the C group and in the D group (53 +/- 5 mg/dL) were observed when compared with group B (44 +/- 3 mg/dL), resulting in a lower ratio of TC/HDL-C (1.5 +/- 0.1). In the groups C and D, there were significant increases (p < 0.05) in the serum concentrations of retinol (26 +/- 5 microg/dL and 58 +/- 18 microg/dL) and a tocopherol (165 +/- 58 microg/dL) and 445 +/- 65 microg/dL). These results allow to conclude that the supplementation with RBD red diminishes the TC, improving the ratio TC/HDL-C. The presence of a monosaturated fatty acid (oleic acid) and the high concentrations of micronutrients (a tocopherol and retinol) in RBD red palm oil, influence favorably the lipid profile of rats with induced hyperlipidemia.     

Modulation of oral squamous cell carcinoma incidence in rats via diet and a novel calcium channel antagonist

An unexpected dose related increase in oral squamous cell carcinomas was observed in a standard 2-year carcinogenicity study with a novel calcium channel blocker, in which Wistar rats received daily doses of 0, 1.5, 7, 20, or 40 mg/kg of the compound mixed with a standard diet containing fibers from barley. This finding was associated with an increased incidence of severe (destructive) periodontitis and the formation of oro-nasal fistulae at the 2 highest doses. Five assays of the compound for genotoxicity were negative indicating that a genotoxic effect was highly improbable. To investigate the underlying pathogenic mechanisms a second 2-year study in the same strain of rats was initiated and the influence of the diet and/or a possible local irritancy by the drug was assessed. In this second study the compound was administered by oral gavage at daily doses of 0, 7, or 40 mg/kg (later reduced to 20 mg/kg due to systemic intolerance) to rats maintained either on the standard diet or on a low fiber diet assumed to be less aggressive in terms of inducing periodontal lesions. Dose dependent gingival overgrowth (a class-related effect) was observed in the incisor and molar teeth area of all treated groups but was independent of the diet used. No oral tumors were found in the standard diet or low fiber diet controls and all treatment groups fed the low fiber diet, whereas in the high-dose group fed the standard diet a total of 8 oral squamous cell carcinomas were detected in association with an increased incidence of severe periodontitis. These results indicate that the increased incidence of squamous cell carcinomas observed upon chronic administration of the compound is not due to a direct tumorigenic effect of the drug. Tumor formation is attributable to severe periodontal disease favored by the diet and class related gingival overgrowth.     

Central dopamine systems and gastric stress pathology in rats

Acute treatments with haloperidol (1 mg/kg), clozapine (10 mg/kg) and metoclopramide (10 mg/kg) significantly facilitated cold-restraint-induced gastric ulcer formation in rats. In addition, haloperidol and clozapine also produced gastric mucosal erosions in non-stressed rats. Bilateral lesions of the ventral tegmental area (VTA) and substantia nigra also aggravated stress ulcerogenesis--VTA lesions also being effective in inducing gastric ulcers in non-stressed rats. Long-term treatment with dopaminergic blockers showed variable effects. Clozapine potentiated the gastric stress pathology, whereas no significant facilitation was observed with haloperidol or metoclopramide. In addition, withdrawal from haloperidol did not influence the gastric ulcer formation when compared to controls. The role of central dopaminergic involvement in gastric stress pathology is discussed in light of the present results.     

Supplementation of dietary vitamins,protein and probiotics on semen traits and immunohistochemical study of pituitary hormones in zinc-induced molted broiler breeders

The purpose of this study was to investigate the effect of dietary vitamin E and vitamin C, probiotics mixture and protein level and their combination on semen quality and immunohistochemical study of some pituitary hormones in male broiler breeders. One hundred and eighty male broiler breeders 65 weeks old were divided into six groups by completely randomized design. The birds were subjected to zinc-induced molt by mixing zinc oxide at the rate of 3000 mg/kg in the feed. After molting, one group was fed control diet (CP16%). The other groups were fed vitamin E (100 IU/kg), vitamin C (500 IU/kg), probiotics (50 mg/L of drinking water), protein (CP14%) and combination of these components. These treatments were given for five weeks. After the feeding period, semen samples were taken and analyzed for semen volume, sperm concentration, motility and dead sperm percentage. Pituitary samples were collected from three birds per replicate and were processed for immunohistochemical study. The results of semen quality parameters revealed that semen volume and sperm motility were significantly high in the vitamin E fed group, while the dead sperm percentage decreased significantly in the vitamin C group. The morphometric analysis revealed that compared to other groups, vitamin E caused a significant increase in the size and area of FSH, LH gonadotropes and lactotropes. These results showed that vitamin E alone may play some role in the enhancement of semen quality and growth of gonadotropes and lactotropes.     

Aluminium administration is associated with enhanced hepatic oxidant stress that may be offset by dietary vitamin E in the rat

It has been proposed that aluminium toxicity may be mediated, at least in part, by free radical generation. We have investigated the effects of aluminium lactate administration on indices of hepatic oxidant stress, and the consequences of concomitant dietary vitamin E, in male albino Wistar rats. Aluminium lactate was administered for 4 weeks, by ip injection at 10 mg aluminium/kg body weight. Groups of animals received a chow diet containing 0, 5, 15, or 20 mg vitamin E/g of food. A control group of rats received a normal chow diet, without being injected with aluminium. The rats were killed after 4 weeks, and blood and liver tissue removed for the measurement of aluminium and markers of oxidative stress. Plasma and liver aluminium levels were increased in all groups of animals receiving aluminium lactate (P < 0.01), although these levels were significantly reduced in rats receiving concomitant vitamin E (P < 0.05). Aluminium treatment was associated with significantly increased levels of hepatic reactive oxygen species (ROS) (P < 0.01) that were attenuated by concomitant vitamin E (P < 0.05). Hepatic catalase and reduced glutathione levels were both reduced in animals treated with aluminium (P < 0.05).     

Estradiol Treatment Ameliorates Acetic Acid-Induced Gastric and Colonic Injuries in Rats

To evaluate the role of estrogen treatment on the healing of acetic acid-induced gastric or colonic injury, rats were given 17beta estradiol benzoate (0.001, 0.1, and 10 mg/kg) or vehicle for 7 days (following the induction of ulcer) or 4 days (following the induction of colitis) until they were decapitated. Food intake and fecal output were decreased by estradiol treatment but gastric emptying rate was not changed. Estradiol (10 mg/kg) reduced gastric ulcer index and colonic damage score compared to vehicle-treated groups. SEM and light microscopy demonstrated a significant reduction in the severity of ulcers and colitis by estradiol treatment. Gastric microscopic score was not changed by estradiol treatment, whereas in the colonic tissue score was significantly reduced. Elevated gastric MPO levels were reduced in gastric but not in colonic tissues as compared with corresponding vehicle groups. In conclusion, exogenous estradiol treatment at pharmacological doses improves the healing of both gastric and colonic injury induced by acetic acid in rats.     

Regulation of antral gastrin content

Five groups of rats were fasted for 3 days and injected with either NaCl or 5, 10, 20, or 40 micrograms/kg bombesin every 8 h. The animals were killed, and their serum and antral gastrin levels were compared with those of normally fed rats. Fasting reduced serum gastrin to 14% of control; antral gastrin was reduced to 21% of control. All doses of bombesin significantly increased serum gastrin in fasted rats, and 20 and 40 micrograms/kg significantly increased antral gastrin. A group of normally fed rats was also compared with one fed a liquid diet for 7 days. Half of each of these was injected with 20 micrograms/kg bombesin (3 times/day) and the other half with NaCl. Bombesin significantly increased serum and antral gastrin in the rats fed solid food. The liquid diet lowered serum and antral gastrin to 17 and 59% of control values, respectively. Bombesin injection totally prevented these decreases. These data indicate that food in the gastrointestinal tract is not required for either gastrin release or synthesis. Furthermore, the data suggest that gastrin synthesis is regulated primarily by gastrin release or by direct stimulation by bombesin rather than by specific food products.     

Effects of amphetamine and phenylpropanolamine on food intake in rats with ventromedial hypothalamic or dorsolateral tegmental damage

Female rats with sham lesions or lesions of the ventromedial hypothalamus (VMH) or the dorsolateral tegmentum (DLT) were maintained at 80% normal body weight to minimize possible group differences in hunger motivation. VMH rats displayed attenuated amphetamine (0.5, 1.0, and 2.0 mg/kg) anorexia when fed a high-fat test diet but normal anorexia when fed a pellet test diet whereas DLT rats displayed attenuated amphetamine anorexia when fed either test diet. Neither VMH nor DLT rats displayed attenuated anorexia to phenylpropanolamine (5.0, 10.0, and 20.0 mg/kg), an analogue of amphetamine. These results are discussed in terms of an amphetamine-activated arousal mechanism within the DLT.     

An interaction between dietary tryptophan and stress in exacerbating gastric disease

Rats fed a tryptophan deficient diet composed of corn developed significantly more gastric erosive disease when subjected to prolonged immobilization than similarly stressed rats fed a tryptophan enriched diet. No gastric disease developed in control groups which were not immobilized. No significant correlations were found between treatment groups and levels of indoleamines in brain and gut. However, serum tryptophan was significantly lowered only in the group of stressed rats fed a tryptophan deficient diet. This report raises the possibility that people eating preponderantly a corn-based diet, deficient in tryptophan, may be at increased risk of having stress ulcer disease of the gut.     

The effect of vitamin E or selenium on the oxidant-antioxidant balance in rats.

Vitamin E and selenium are two components which contribute to the antioxidant potential of plasma and tissues. In the present study we aimed to define the type of tissue toxicity deriving from chronic deficiency of either vitamin E or selenium and to evaluate the reliability of peripheral markers of tissue toxicity in these conditions. We studied rats fed a vitamin E or selenium-deficient diet for 3 or 7 months and a selenium-supplemented diet. The effectiveness of the dietary treatment was confirmed by measuring vitamin E and selenium in plasma. Heart and kidney malondialdehyde (MDA), a typical product of lipid peroxidation, was significantly increased after the 3-month diet in both vitamin E- and selenium-deficient rats. The iron-binding capacity of plasma, an activity ascribed to plasma transferrin, was reduced in selenium-deficient and increased in selenium-supplemented animals. In red cells globular resistance (resistance to osmotic haemolysis) was low in vitamin E- and selenium-deficient, but high in selenium-supplemented animals. Glutathione peroxidase was also increased in selenium-supplemented rats. Platelet count did not differ from controls in any of the three conditions studied. Platelet MDA formation induced by arachidonic acid was raised in both selenium-deficient and, particularly, vitamin E-deficient groups. This can be regarded as a peripheral marker of reduced antioxidant defence at tissue level.