Oxidative stress modulates membrane bound ATPases in brain regions of PCB (Aroclor 1254) exposed rats: protective role of alpha-tocopherol.

Polychlorinated biphenyls (PCBs) are a class of widely dispersed and environmentally persistent organic compounds. PCBs exhibit a wide range of toxicological effects including neurotoxicity. Vitamin E (alpha-tocopherol) is an important lipid soluble antioxidant placed in a special region of membranes. Large amounts of energy are required to maintain the signaling activities of the cells in the central nervous system (CNS). Membrane proteins that control ion gradients across organellar and plasma membranes appear to be particularly susceptible to oxidation-induced changes. The aim of this study was to determine the protective role of vitamin E on Aroclor 1254 induced modulation in membrane bound ATPases in brain regions of rats. One group of rats received corn oil as vehicle for 30days as control. The other group of rats were administered Aroclor 1254 at a dose of 2mgkg(-1) bwday(-1) intraperitoneally for 30days. One group of rats received vitamin E (50mgkg(-1) bwday(-1)) orally simultaneously with Aroclor 1254 for 30days. After 30days, the animals were euthanized and the brain was dissected to hypothalamus and hippocampus to determine the following parameters. Hydrogen peroxide (H2O2), Lipid peroxidation (LPO) and the activities of Na+K+-ATPase, Ca2+-ATPase and Mg2+-ATPase were determined. Reduced glutathione (GSH) level was also determined. Activities of all the enzymes were decreased while an increase in H2O2 and LPO were observed in selected brain regions of PCB treated animals. Simultaneous vitamin E treatment in PCB exposed animals restored all the parameters significantly. These results suggest that oxidative stress is involved in the inhibitory effect of PCB (Aroclor 1254) on membrane bound ATPases in selected brain regions. alpha-tocopherol acts against PCB induced neurotoxicity by decreasing oxidative stress.     

Chronic cold exposure affects the antioxidant defense system in various rat tissues

BACKGROUND: Chronic exposure to stress alters the normal body homeostasis and, hence, leads to the development of various human pathologies, which might involve alterations in the antioxidant defense system. We studied the effect of chronic cold exposure on oxidative stress and antioxidant defense system in various rat tissues. METHODS: Male albino rats (Wistar strain), 2-3 months old, were exposed to 3 weeks of cold treatment. Antioxidant enzymes, superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), glutathione reductase (GR) and glutathione S-transferase (GST) were measured in addition to the antioxidants, ascorbic acid (AsA) and glutathione (GSH), and the prooxidants, lipid peroxides (LPO) and xanthine oxidase (XOD), in brain, heart, kidney, liver and small intestine using standard protocols. RESULTS: Chronic cold exposure resulted in a significant increase in LPO in all the tissues studied while XOD was increased in the brain and intestine. Total SOD activity was significantly decreased in all the tissues, whereas CAT activity was significantly increased in the kidney and decreased in heart, liver and intestine in the animals exposed to cold. GPx activity was increased only in the brain and intestine of stressed rats. Chronic cold exposure resulted in significant decrease in GR activity in heart, liver and intestine. GST activity was increased (except heart) and GSH was significantly decreased in all the tissues in treated rats. AsA was increased in kidney and intestine but decreased in heart of stressed animals. CONCLUSIONS: The observed changes in the antioxidant defense system are tissue specific, but it is evident that chronic exposure to cold leads to oxidative stress by displacing the prooxidant-antioxidant balance of this defense system by increasing the prooxidants while depleting the antioxidant capacities.     

Stabilization of pulmonary mitochondrial enzyme system by capsaicin during benzo(a)pyrene induced experimental lung cancer

The modulatory efficacy of capsaicin on lung mitochondrial enzyme system with reference to mitochondrial lipid peroxidation (LPO), antioxidants, key citric acid cycle enzymes and respiratory chain enzymes during benzo(a)pyrene (B(a)P) induced lung cancer in Swiss albino mice was studied. Elevations in mitochondrial LPO along with decrements in enzymic antioxidants (superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), glutathione reductase (GR) and glutathione-S-transferase (GST)), non-enzymic antioxidants (reduced glutathione (GSH), vitamin C, vitamin E and vitamin A), citric acid cycle enzymes (isocitrate dehydrogenase (ICDH), alpha-ketoglutarate dehydrogenase (alpha-KDH), succinate dehydrogenase (SDH) and malate dehydrogenase (MDH)), and respiratory chain enzymes (NADH dehydrogenase and Cytochrome c oxidase) were observed in B(a)P (50mg/kg body weight) administered animals. CAP (10mg/kg body weight) pretreatment decreased lung mitochondrial LPO and augmented the activities of enzymic, non-enzymic antioxidants, citric acid cycle enzymes and respiratory chain enzymes to near normalcy revealing its chemoprotective function during B(a)P induced lung cancer.     

Protective effects of vitamin C, alone or in combination with vitamin A, on endotoxin-induced oxidative renal tissue damage in rats

This study was designed to investigate the protective effects of vitamin C and vitamin A on oxidative renal tissue damage. Male Wistar rats were given an intraperitoneal injection of 0.5 ml saline (control) or 0.5 ml solution of lipopolysaccharide (10 mg/kg), which caused endotoxemia. Immediately (within 5 min) after the endotoxin injection, the endotoxemic rats were untreated or treated with intraperitoneal injection of vitamin A (195 mg/kg bw), vitamin C (500 mg/kg bw) or their combination. After 24 hours, tissue and blood samples were obtained for histopathological and biochemical investigation. Endotoxin injection caused renal tissue damage and increased erythrocyte and tissue malondialdehyde (MDA) and serum nitric oxide (NO), urea and creatinine concentrations, but decreased the superoxide dismutase (SOD), glutathione peroxidase (GSH-Px) and catalase (CAT) activities compared to the parameters of control animals. Treatment with vitamin C or with vitamins C and A significantly decreased the MDA levels and serum NO, urea and creatinine levels, recovered the antioxidant enzyme activities (SOD, GSH-Px and CAT), and prevented the renal tissue damage in endotoxemic rats. In contrast, vitamin A alone did not change the altered parameters except for creatinine levels. Notably, the better effects were observed when vitamins A and C given together. It is concluded that vitamin C treatment, alone or its combination with vitamin A, may be beneficial in preventing endotoxin-induced oxidative renal tissue damage and shows potential for clinical use.     

Endocrine disruptive effects of polychlorinated biphenyls on the thyroid gland in female rats

Polychlorinated biphenyls (PCBs) are persistent environmental pollutants. Aroclor 1221 (A1221) and Aroclor 1254 (A1254) are commercial PCB mixtures with low and high number of chlorination, respectively. We have comparatively investigated effects of A1221 and A1254 on serum levels of thyroid hormones and thyroid gland histology in adult female Wistar rats. Animals were subcutaneously injected with A1221 (10 mg/kg) or A1254 (10 mg/kg) for six weeks. One group of animals served as control. At the end, all animals were decapitated and trunk blood collected. Serum levels of triiodothyronine (T3) and thyroxine (T4) were measured by the electrochemiluminescence immunoassay method. Thyroid glands were removed for histopathological examination under light microscopy. Serum total T4 levels were significantly increased in A1221- and A1254-treated rats (p < 0.05). Serum free T4 levels were significantly increased in the A1254-treated rats (p < 0.01), but not in the A1221-treated rats. In contrast, the treatment with A1221 caused a significant increase in serum free T3 concentrations (p < 0.05) but not with A1254. Notably, either A1221 or A1254 caused distinct histopathological changes, such as formation of many microfollicles in the thyroid gland, which mimic the changes seen in thyrotoxicosis. In conclusion, both PCB mixtures induce toxic effects in the thyroid gland regardless of their degree of chlorination. We suggest that these environmental contaminants may disrupt thyroid hormone homeostasis in exposed individuals and thus pose a threat to human health.     

The modulatory effect of deltamethrin on antioxidants in mice

BACKGROUND: Deltamethrin is a alpha-cyano pyrethroid insecticide used extensively in pest control. Although initially thought to be least toxic, a number of recent reports showed its toxicity in mammalian and non-mammalian laboratory and wildlife animal species. In fish, it is a potent oxidative stress-inducing agent. We studied the oxidative stress-inducing effect of deltamethrin in mice. METHODS: Male Swiss albino mice were orally administered 2 doses of deltamethrin viz., 5.6 and 18mg/kg body weight (bw), for 15 days. RESULTS: Both the doses of deltamethrin significantly induced lipid peroxidation (LPO) in liver and kidney. Along with the induction of LPO, activities of vital antioxidant enzymes such as glutathione peroxidase (GPx), glutathione S-transferase (GST) and catalase (CAT) were also suppressed in both the tissues. Glutathione (GSH) level was also decreased. GSH decrease was more pronounced in kidney than the liver. CONCLUSION: Toxicity of many chlorinated and organophosphate insecticides is mediated by the reactive oxygen species (ROS). Findings of the present investigation also suggest a role for ROS in deltamethrin toxicity. An increased LPO indicates that these ROS might have caused degradation of biomembrane in deltamethrin-exposed animals.     

Pongamia pinnata modulates the oxidant-antioxidant imbalance in ammonium chloride-induced hyperammonemic rats

The effect of Pongamia pinnata (an indigenous plant used in Ayurvedic Medicine in India) leaf extract (PPEt) on circulatory lipid peroxidation and antioxidant status was evaluated in ammonium chloride-induced hyperammonemic rats. Enhanced lipid peroxidation in the circulation of ammonium chloride-treated rats was accompanied by a significant decrease in the levels of vitamin A, vitamin C, vitamin E, reduced glutathione (GSH), glutathione peroxidase (GPx), superoxide dismutase (SOD), and catalase (CAT). PPEt-administered rats experienced a significant reduction in lipid peroxidation with a simultaneous elevation in antioxidant levels. Our results indicate that PPEt modulates these changes by reversing the oxidant-antioxidant imbalance during ammonium chloride-induced hyperammonemia and this could be due to its (i) antihyperammonemic effect by means of detoxifying excess ammonia, urea and creatinine and (ii) antioxidant property. The exact mechanism has to be still investigated and isolation of active constituents is required.     

Lipid profile, oxidant-antioxidant status and glycoprotein components in hyperlipidemic patients with/without diabetes

BACKGROUND: Plasma lipoproteins are protected against oxidative modification by the antioxidant defense system. An imbalance in the antioxidant defense system seems to result from the accumulation of low density lipoprotein (or) very low density lipoprotein in the course of hyperlipidemia. METHODS: The lipid profile, glycoprotein components, glucose, total proteins, albumin, lipid peroxidation and antioxidant status of plasma and erythrocytes were investigated in hyperlipidemic patients and hyperlipidemic patients with diabetes on treatment with glibenclamide (or) glipizide along with normal subjects and compared. RESULTS: A significant increase was observed in the levels of total cholesterol (TC), VLDL-C, triglycerides (TG), lipid peroxidation, ceruloplasmin (CP), glycoprotein components and glucose in the hyperlipidemic patients with/without diabetes and the increase was more pronounced (except TC) in patients with diabetes. The activities of erythrocyte antioxidant enzymes such as superoxide dismutase (SOD), glutathione peroxidase (GPx), catalase (CAT) and plasma concentrations of vitamins C and E, and reduced glutathione (GSH) decreased in hyperlipidemic patients with/without diabetes. GPx, CAT, vitamin C and GSH levels exhibited a further decrease in hyperlipidemic patients with diabetes. CONCLUSION: An enhanced levels of VLDL-C, TC/HDL-C ratio, TG, lipid peroxidation, glycoprotein components, and decreased concentrations of total proteins (TPs) and albumin were observed in hyperlipidemic patients with diabetes while the decrease was more marked in GSH, vitamin C, CAT and GPx among antioxidants.     

Elevation by Oxidative Stress and Aging of Hypothalamic-Pituitary-Adrenal Activity in Rats and Its Prevention by Vitamin E

The present study was conducted in order to determine whether oxidative stress during aging involves dysfunction of the hypothalamic-pituitary-adrenal (HPA) axis in association with the emergence of cognitive deficits. When young rats were subjected to oxidative stress in the form of hyperoxia, thiobarbituric acid reactive substances, conjugated diene and lipid hydroperoxides increased markedly in the HPA axis. Vitamin E inhibited such increases in lipid peroxides in each organ. Levels of corticotrophin-releasing hormone in the hypothalamus and plasma levels of adrenocorticotrophic hormone and corticosterone were markedly elevated in young rats exposed to hyperoxia. However, young rats fed vitamin E-supplemented diets showed no abnormal hormone secretion, even after being subjected to hyperoxia. Furthermore, glucocorticosteroid receptors (GR) in pyramidal cells in the Cornus ammonis 1 region of the hippocampus in young rats were markedly decreased by oxidative stress. Similar phenomena were also observed in normal aged rats and young rats fed vitamin E-deficient diet kept in a normal atmosphere. Vitamin E supplementation prevented the decrease in GR in the hippocampus and the increase in corticosterone secretion caused by hyperoxia. These results suggest that oxidative stress induces oxidative damage in the hippocampus and the HPA axis during aging, resulting in a cognitive deficit in rats, and that negative-feedback inhibition on HPA activity was markedly dampened due to an increase in corticosterone levels caused by loss of GR.     

Chemopreventive efficacy of ginger, a naturally occurring anticarcinogen during the initiation, post-initiation stages of 1,2 dimethylhydrazine-induced colon cancer

BACKGROUND: Ginger (Zingiber officinale Rosc) is a natural dietary component, which has antioxidant and anticarcinogenic properties. We investigated the effect of ginger on the initiation and post-initiation stages of 1,2-dimethylhydrazine (DMH)-induced colon carcinogenesis in male Wistar rats. METHODS: Rats were given a weekly subcutaneous injection of DMH (20 mg/kg body weight) in the groin for 15 weeks. Ginger (50 mg/kg body weight/everyday p.o.) was given to the rats at the initiation, post-initiation stages of carcinogenesis. The activity of lipid peroxidation was studied by measuring the formation of thiobarbituric acid reactive substances (TBARS), lipid hydroperoxides (LOOH) and conjugated dienes (CD), and the antioxidant status by measuring superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPX), glutathione-S-transferase (GST), glutathione reductase (GR), reduced glutathione (GSH), vitamins C, E, and A concentrations in the circulation of 1,2-dimethylhydrazine-induced experimental colon cancer. RESULTS: In the presence of a known colon carcinogen, DMH, plasma lipid peroxidation (TBARS, lipid hydroperoxides and conjugated dienes) and cancer incidence were significantly increased whereas enzymic (GPx, GST, GR, SOD and CAT) and non-enzymic antioxidant concentrations (GSH, vitamins C, E, and A) were decreased as compared to control rats. The number of tumors as well as the incidence of cancer was significantly decreased on treatment with ginger. In addition, ginger supplementation at the initiation stage and also at the post-initiation stages of carcinogenesis significantly reduced circulating lipid peroxidation and significantly enhanced the enzymic and non-enzymic antioxidants as compared to unsupplemented DMH-treated rats. CONCLUSIONS: Ginger supplementation suppresses colon carcinogenesis in the presence of the procarcinogen DMH.     

Antioxidant and antitumor efficacy of Luteolin,a dietary flavone on benzo(a)pyrene-induced experimental lung carcinogenesis

The present study is designed to assess the antioxidant and antitumor potential of luteolin against benzo(a)pyrene [B(a)P]-induced lung carcinogenesis in Swiss albino mice. Here, we reported that oral administration of B(a)P (50 mg/kg body weight) to mice resulted in raised lipid peroxides (LPO), lung specific tumor markers such as carcinoembryonic antigen (CEA) and neuron specific enolase (NSE) with concomitant decrease in the levels of both enzymatic antioxidants such as superoxide dismutase (SOD), catalase (CAT), glutathione reductase (GR), glutathione peroxidase (GPx) and glutathione-s-transferase (GST), and non-enzymatic antioxidants such as reduced glutathione (GSH), vitamin E and vitamin C. Luteolin treatment (15 mg/kg body weight, p.o) significantly counteracted all these alterations and maintained cellular normalcy. Moreover, assessment of protein expression levels by western blot analysis revealed that luteolin treatment effectively negates B(a)P-induced upregulated expression of proliferating cell nuclear antigen (PCNA), cytochrome P450 1A1 (CYP1A1) and nuclear factor-kappa B (NF-κB). Furthermore, histopathology of lung tissue and immunohistochemistry of CYP1A1 were carried out to substantiate the anti- lung cancer effect of luteolin. Overall, these findings confirm the chemopreventive potential of luteolin against B(a)P induced lung carcinogenesis.     

Lower doses of vanadate in combination with trigonella restore altered carbohydrate metabolism and antioxidant status in alloxan-diabetic rats

BACKGROUND: Vanadate treatment to diabetic rats has been reported to correct the altered carbohydrate metabolism and antioxidant status. However, vanadate exerts these effects at relatively high doses and several toxic effects are produced. We used low doses of vanadate in combination with Trigonella foenum graecum seed powder (TSP) and evaluated their effect on the enzyme changes in diabetic rats. METHODS: Alloxan-diabetic rats were treated separately with insulin, vanadate (0.6 mg/ml), TSP and a combined dose of Vanadate (0.2 mg/ml) and TSP for 21 days. At the end of the experimental period, blood glucose levels and activities of pyruvate kinase (PK), phosphoenolpyruvate carboxykinase (PEPCK), glutathione peroxidase (GPx), glutathione reductase (GR), superoxide dismutase (SOD) and catalase (CAT) were measured in cytosolic fraction in the liver and kidney. RESULTS: Blood glucose levels increased markedly in diabetic rats. Treatment with antidiabetic compounds resulted in the reduction of glucose levels. Rats treated with combined dose of vanadate and trigonella had glucose levels comparable to control ones. Similar results were obtained with the activities of PK, PEPCK, SOD, GPx, GR, and CAT in liver and kidney of diabetic rats. Combined dose of vanadate and Trigonella was found to be most effective in correcting these alterations. CONCLUSIONS: Lower doses of vanadate could be used in combination with TSP to effectively counter diabetic alterations without any toxic side effects.     

Ovariectomy induces oxidative stress and impairs bone antioxidant system in adult rats

BACKGROUND: There is increasing evidence suggesting the role of free radicals in bone resorption and bone loss. Ovariectomized rats have been used as the animal model for the study of osteoporosis. Oxidative stress due to reactive oxygen species (ROS) can cause oxidative damage to cells. Cells have a number of defense mechanisms to protect themselves from the toxicity of ROS. Even though, there are studies portraying the role of free radicals in bone loss, the defense mechanism adapted by bone in ovariectomized animals remains obscure. We investigated the impact of ovariectomy (OVX) on the bone antioxidant system in rats. METHODS: Sixty days after bilateral OVX, the rats were killed and the femora were removed, the tissue homogenates were made and used for the estimation of superoxide dismutase (SOD), glutathione peroxidase (GPx), glutathione S transferase (GST), lipid peroxidation (LPO) and hydrogen peroxide (H(2)O(2)). RESULTS: The levels of LPO and H(2)O(2) were increased and enzymatic antioxidants like SOD, GPx, GST were decreased in ovariectomized animals when compared to sham-operated control rats. The calculated correlation coefficient demonstrated strong correlation (0.905) between the production of H(2)O(2) and LPO in the femur bone. A strong inverse (-0.945) correlation was observed between H(2)O(2) production and SOD activity. CONCLUSIONS: OVX induces oxidative stress in the femur bone of rats.     

Evaluation of Acetamiprid Mediated Oxidative Stress and Pathological Changes in Male Rats: Ameliorative Effect of Curcumin

Present study was undertaken to evaluate the acetamiprid-mediated toxicity and possible protective effect of curcumin in rats. Rats were divided into seven different groups. They received curcumin (100 mg/kg, b.wt. p.o.) and acetamiprid (26.25 and 105 mg/kg b.wt., p.o.) alone and in their combinations for period of 28 days. Lipid peroxidation and antioxidant enzyme activities were determined in liver, kidney and brain and cellular changes histopathologically. Study shows that administration of acetamiprid caused a significant induction in oxidative damage in liver, kidney and brain as evidenced by increased level of lipid peroxidation (LPO) and altered activities of reduced glutathione (GSH), catalase (CAT), superoxide dismutase (SOD) and glutathione reductase (GR). Co-administration of curcumin with acetamiprid significantly decreased LPO, caused marked restoration in the non-enzymatic (GSH) and enzymatic antioxidants system (CAT, SOD and, GR) and protected from acetamiprid-mediated structural alterations of liver, kidney and brain. The results of present study indicates that curcumin ameliorate the acetamiprid-induced toxic damage to vital organ mediated via oxidative stress.

     

Decrease in antioxidant status of plasma and erythrocytes from patients with ankylosing spondylitis

ObjectivesThe aim of the study was to evaluate the antioxidant status in plasma and erythrocytes from patients with ankylosing spondylitis (AS).Methods16 patients with AS and 16 healthy volunteers were involved in this study. Activities of antioxidant enzymes: superoxide dismutase (SOD) and its isoenzymes — (SOD-Mn) and (SOD-ZnCu), catalase (CAT), glutathione peroxidase (GPx), glutathione reductase (GR) and glutathione transferase (GST), as well as the total antioxidant status (TAS) and concentration of malondialdehyde (MDA) in plasma and/or erythrocytes, respectively were determined.ResultsIn patients with AS, a statistically significant decrease in plasma activity of SOD, SOD-CuZn and TAS, significant drop in activity of SOD, GPx, GST and GR in erythrocytes, as well as increased concentration of MDA in comparison with control group of healthy volunteers was observed.ConclusionDecrease in antioxidant status leading to generation of oxidative stress may play an important role in the pathogenesis of ankylosing spondylitis.     

Effect of vitamin E and vitamin C supplementation on antioxidative state and renal glomerular basement membrane thickness in diabetic kidney

The aim of this study was to analyze the effect of vitamins C and E on malondialdehyde (MDA) content and activities of key antioxidant enzymes: superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GSH-Px) as well as glomerular basement membrane (GBM) thickness in streptozotocin-induced diabetic kidney in rats. Wistar male rats were divided into following groups (12 rats each): the control, diabetic rats, diabetic rats whose drinking water was supplemented with vitamin C in a dose of 1.0 g/l or diet was supplemented with 200 mg of vitamin E/100 g fodder. Body weight, blood glucose and HbA1C levels and 24-hour urinary albumin excretion (UAE) were studied every week (0-12 weeks). After 6 and 12 weeks, MDA content and activities of SOD, CAT and GSH-Px were measured in the kidney homogenate supernatants. Electron micrographs of glomeruli were scanned and morphometric investigations were performed by means of computer image analysis system to compare GBM thickness. The blood glucose and HbA1C concentrations and UAE in diabetic rats were significantly higher than in the control group. An increase in the MDA level and decrease in the SOD, CAT and GSH-Px activities in the kidney of diabetic rats were observed after 6 and 12 weeks of experiment. Administration of vitamins C and E did not affect body weight, blood glucose and HbA1C levels. Both vitamin C and vitamin E decreased lipid peroxidation and augmented the activities of antioxidant enzymes studied in the kidneys of diabetic rats as well as reduced UAE, decreased kidney weight and GBM thickness. The results indicate the potential utility of antioxidant vitamins in the protection against the development of diabetic nephropathy.     

Effect of hemodialysis on the oxidative stress and antioxidants.

Oxidative stress plays a role in many disease states. These diseases have an increased incidence in uremia, and particularly in hemodialysis (HD) patients. This suggests an increased exposure to oxidative stress. An imbalance between oxidants and antioxidants has been suggested in uremic patients on HD. However, the respective influence of uremia and dialysis procedure has not been evaluated. It is postulated that antioxidant capacity in uremic patients is reduced, yet the mechanism remains unclear. We have determined the levels of lipid peroxidation expressed as thiobarbituric acid-reactive substances. We assessed oxidative protein damage by carbonyl content and activities of antioxidant enzymes including superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPx) in predialysis uremic patients and in end-stage renal disease (ESRD) patients before and after hemodialysis. Vitamin E and vitamin C levels, reduced glutathione and sulfhydryl content were also studied. We found enhanced oxidative stress in ESRD patients undergoing HD and in predialysis uremic patients. This was mostly due to defective antioxidant enzyme levels. Preventive modalities, including use of biocompatible membranes, ultrapure dialysate, exogenous supplementation of antioxidant vitamins, extracorporeal removal of reactive oxygen species (ROS) and oxidatively modified substances, would appear highly desirable to reduce complications in the long-term dialysis patients.     

Correlation of oxidative status with BMI and lung function in COPD

OBJECTIVES: The imbalance in oxidative status together with nutrition depletion and low body weight play a vital role in the pathogenesis and severity of chronic obstructive pulmonary disease (COPD). The study was undertaken to ascertain if a relationship existed between oxidative status and BMI in COPD. In addition, association of oxidative status and BMI with lung function of the disease was also examined. MATERIALS AND METHODS: In 202 COPD patients and 136 healthy controls plasma lipid peroxidation (LPO), reduced glutathione (GSH), glutathione peroxidase (GPx), catalase (CAT) activities, BMI and FEV(1)% predicted were looked for interactions. RESULTS: The patients had increased LPO (p=0.006) and decreased antioxidants (GSH, p=0.005; GPx, p=0.035 and CAT, p=0.008, respectively). Of note are the correlations of oxidative stress markers with BMI and FEV(1)% predicted in the patients. LPO inversely and GSH, GPx, and CAT positively correlated with both BMI (p=0.007, p<0.001, p=0.045 and p=0.009, respectively), and FEV(1)% of predicted (LPO, p=0.001; GSH, p<0.001; GPx, p=0.043 and CAT, p<0.001) in the patients. Further, a positive correlation existed between BMI and FEV(1)% predicted (p=0.016) in COPD. CONCLUSION: The intimate relationship of oxidative status with BMI and lung function, and the direct correlation between BMI and FEV(1) may potentiate severity of the disease.     

Effects of vitamin E deficiency on the hormone secretion of the pituitary-gonadal axis of the rat

Chronological changes of gonadotropin (FSH and LH) and testosterone concentrations in the serum were measured in vitamin E deficient rats to investigate the effects of vitamin E deficiency on the pituitary-gonadal function in rats. The receptor sites and association constant (Ka) for LH and the formation of cyclic AMP in the Leydig cells were also investigated. The results obtained in the present study are as follows: 1) The vitamin E deficient rats showed almost complete hemolysis and extremely increased TBA reacting substances (TBARS) in the serum and liver. 2) The serum LH concentration in the vitamin E deficient group was slightly higher than in the vitamin E supplemented group during the later periods of experiment. 3) The serum FSH concentration in the vitamin E deficient group did not differ significantly from that in vitamin E supplemented group, but became significantly higher than that in the latter at 186 days of experiment. 4) The serum testosterone concentration was always lower in the vitamin E deficient group than in the control. 5) The vitamin E deficient group showed slightly large number of LH/hCG receptor and significantly small Ka (low affinity), as compared with vitamin E supplemented group. The formation of cyclic AMP by Leydig cells decreased significantly in vitamin E deficient group. These results suggest that the vitamin E deficiency exerted a suppressive effect directly on the gonadal function to decrease the hormone synthesis in the Leydig cells and caused the increased secretion of pituitary LH owing to the feedback mechanism.     

Ameliorative effects of dietary caloric restriction on oxidative stress and inflammation in the brain of streptozotocin-induced diabetic rats

BACKGROUND: There is a strong association between oxidative stress and inflammation in the pathologies of diabetes. Recent evidence suggests that these phenomena could impair brain function. We investigated the potential role of dietary caloric restriction in ameliorating the effects of both oxidative stress and inflammation in the brain of streptozotocin-induced type 2 diabetic rats. METHODS: Forty male Wistar rats were subjected to 30% caloric restriction (20 animals) and ad libitum feeding (20 animals) for 9 weeks before the induction of diabetes in 20 animals (10 from each group) by intraperitoneal injection of 35 mg/kg body weight streptozotocin. RESULTS: Caloric restriction was able to significantly (p>0.05) reduce triglyceride, ROS, IL6, TNF-alpha and body weights in diabetic rats. However, no significant differences were obtained in the antioxidant enzyme (SOD, CAT and GPx) activities except in GPx where caloric restriction increased the levels in both non-diabetic and diabetic rats. CONCLUSION: Caloric restriction was found to ameliorate the oxidative and inflammatory effects of diabetes in the brain. Non-diabetic rats feeding ad libitum were found to have increased levels of oxidative stress and inflammatory biomarkers and these could, in part, be due to their increased body weights.