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At least 19 recordsLinked to original sources

Maharishi Amrit Kalash rejuvenates ageing central nervous system's antioxidant defence system: an in vivo study.

The oxygen-free radical involvement in various deteriorative processes and in ageing is unquestionably established. In the present study age-related changes in antioxidant enzyme activity in the different regions of CNS of 10-month and 32-month-old guinea pigs were studied. Maharishi Amrit Kalash has shown promise in inhibiting the in vitro and in vivo lipid peroxidation. Therefore in the present study the effect of MAK on the activity of antioxidant enzymes was checked. Our results indicate that the activity of superoxide dismutase and glutathione peroxidase, was found to be reduced (P < 0.05) in all the regions of CNS studied, The activities of catalase declined significantly only in the cerebral cortex, hypothalamus and the cerebellum. Whereas glutathione reductase activity declined in the cerebral cortex and hypothalamus. It is concluded that the age-related decline in the activities of antioxidant enzymes is region-specific as well as enzyme-specific. The endogenous lipid peroxide was found to be increased significantly (P < 0.05) in the 32-month-old animals. Whereas the lipid peroxidation after incubating the tissue homogenate in the air was found to be decreased (P < 0.05) in the older animals. The results indicate that the accumulation of lipid peroxides take place with age but the susceptibility of lipid peroxidation decreases in the older animals. The treatment of MAK 500 mg kg-1 body wt. for 2 months could augment the activities of antioxidant enzymes (P < 0.05). The effect of MAK was more pronounced in older than younger animals. It is concluded that the MAK can be used in compensating the decline in the activities of antioxidant enzymes in CNS and thereby it reduces the risks of lipid peroxidation.

Aging↗

Chemo-defence system.

By analogy with the immune defence system, the existence is suggested of a chemo-defence system protecting living organisms against toxic substances, whether natural or man-made, that are present in the environment. This paper deals first with the various facets of such a system: mechanisms involving, among others, lipophilic compounds, hydrophilic compounds, oxidants, acidosis, genotoxics and metals; second, with the biological characteristics of the system and a comparison with the immune defence system: partial immaturity of the young, inducibility, non-specificity and specificity, and saturability; we will show that the two systems share many common features; third, with the evolution of the system, which demonstrates that the system is very old and suggesting that it came into existence before the immune defence system; and fourth, with some of its consequences: estimation of the 'toxic effects' of low doses, hormesis, impact of a vegetable diet on health. Finally, it could be emphasised that life is well protected against chemicals by its chemo-defence system, which appeared very early with the first living organisms on the earth.

Biotransformation↗

Specific and non-specific parameters of the host defence system in patients with superficial fungal infections.

Some measures of systemic host defences, i.e. white cell counts, lymphocyte subsets, delayed-type hypersensitivity and polymorphonuclear leucocyte functions, were evaluated in 42 patients suffering from cutaneous superficial mycoses and in 35 healthy volunteers. Patients were divided according to the extent of their lesions into two groups: group A (30 patients) with skin involvement > or = 30% and group B (12 patients) with skin involvement < or = 1%. No significant abnormalities in systemic defence mechanisms were observed in group B patients, whereas multiple alterations of polymorphonuclear phagocyte activities, i.e. chemotaxis, phagocytosis, mitogen-induced superoxide anion production, were observed in patients with extensive lesions. The values of these phagocytic functions remained significantly reduced (P < 0.01) in these patients after recovery and during a 6-month follow-up period.

Adolescent↗

CRISPR-Cas regulates expression of embedded anti-phage defence systems.

Bacteria utilize diverse defence systems to protect against harmful foreign DNA such as bacteriophages1,2, but how these systems coordinate with each other remains poorly understood. Here we uncover CRISIS (CRISPR-supervised immune system), a widespread regulatory paradigm whereby type I CRISPR-Cas loci embed and transcriptionally modulate diverse innate defences. Small non-canonical CRISPR RNA (crRNA)-like RNAs guide the I-C CRISPR-associated complex for antiviral defence (Cascade) effector complex to inhibit promoters of diverse immune cassettes-including composite multi-system clusters-enabling their basal expression for antiviral activity while mitigating fitness costs associated with hyperactivation, such as host growth impairment or exclusion of beneficial plasmids. When CRISPR-Cas is compromised by mutation or anti-CRISPR proteins, there is a burst in transcription of these embedded defence systems, leading to higher-level innate immunity at the expense of host fitness. Together, adaptive CRISPR-Cas systems orchestrate diverse innate immune systems into a layered defence network, comprising a prokaryotic 'immunity guard' strategy.

Bacteriophages↗

Why do bacteria accumulate antiphage defence systems?

While it is well established that bacterial genomes encode multiple and diverse antiphage systems, the reasons for their co-occurrence and their heterogeneous distribution remain debated. This review examines why bacteria accumulate antiphage systems and how this influences phage-bacteria interactions, particularly in the context of phage therapy. Two main hypotheses may explain this phenomenon: (i) the pan-immunity hypothesis, which suggests that defence system accumulation provides protection against phage predation at the community level, and (ii) mobile genetic element (MGE) competition, where defence systems primarily protect intra-bacterial MGEs against other ones rather than the bacterial host itself. The ecological context also influences the distribution of antiphage systems, with defencee accumulation shaping phage-bacteria interactions in diverse communities but playing a lesser role at the species level, potentially explaining why multiple defences do not strongly limit phage host range in therapeutic settings. Finally, we address the challenges in understanding the drivers shaping the distribution of defence systems across bacterial genomes (expressions, costs, etc.) and their implications for elucidating the ecological role of defence systems and optimizing phage therapy strategies.This article is part of the discussion meeting issue 'The ecology and evolution of bacterial immune systems'.

Bacteria↗

Virgin olive and fish oils enhance the hepatic antioxidant defence system in atherosclerotic rabbits.

BACKGROUND & AIMS: In this study we report the effects of sunflower, virgin olive and fish oils on the lipid profile and antioxidant defence system in liver mitochondria from rabbits with experimental atherosclerosis. METHOD: An atherogenic control group were fed for 50 days on a diet containing 3% lard and 1.3% cholesterol. Four groups were fed for an additional period of 30 days with a diet enriched in different oils: sunflower oil, virgin olive oil, refined olive oil and fish oil. A control group was fed with a standard chow. RESULTS: The atherogenic diet caused important changes in the hepatic mitochondria lipid profile and in the enzymatic and non-enzymatic antioxidant defence system accompanied with an increase in the content of hydroperoxides in liver mitochondria. The administration of virgin olive and fish oils showed a better profile in the antioxidant system as well as decrease in the content of hydroperoxides. CONCLUSIONS: The intake of cholesterol- and lard-enriched diet leads to a high impairment in the hepatic antioxidant defence system. However, the replacement of that diet by other unsaturated fat-enriched diets using virgin olive, sunflower and fish oil enhances hepatic antioxidant defence system, virgin olive and fish oil diet provide the best results.

Animals↗

Role of catalase in retinal antioxidant defence system: its comparative study among rabbits, guinea pigs, and rats.

The role of catalase in the retinal antioxidant defence system was examined in rabbits, guinea pigs, and rats with and without prolonged administration of a diet containing 0.4% 3-aminotriazole (3-AT), a catalase inhibitor. When weanling rabbits, guinea pigs, and rats we administered 3-AT for 8, 7, and 10 weeks, respectively, retinal catalase activity was reduced by approximately 50% in all these animals. In the retina of rabbits with 3-AT administration, a decrease in superoxide dismutase (SOD) activity and an increase in lipid peroxide (LPO) concentration occurred. while glutathione peroxidase (GSH-px) activity did not change. In the retina of guinea pigs with 3-AT administration, an increase in LPO concentration occurred, while SOD and GSH-px activities did not change. In the retina of rats with 3-AT administration, a decrease in GSH-px activity and an increase in LPO concentration occurred, while SOD activity did not change. An increase in serum LPO concentration was found in rats with 3-AT administration, while the concentration did not change in rabbits and guinea pigs. These results indicate that catalase plays an important role in the retinal antioxidant defence system, but that the way catalase contributes to the maintenance of the retinal antioxidant defence system is different among these animals. The present results suggest that under the prolonged inhibition of catalase, the retina of rats, but not of rabbits and guinea pigs, may suffer from the influence of systemic oxidative stress.

Amitrole↗

Enzymes of oxidant defence system of leucocytes and erythrocytes in bovine anaplasmosis.

The glutathione oxidant defence system in leucocytes and erythrocytes of six Anaplasma marginale-infected calves was examined by assaying glutathione peroxidase (GSH-px), glutathione reductase (GSSG-R), reduced glutathione (GSH) and superoxide dismutase (SOD). In addition, GSH-S-transferase and arginase levels were measured in leucocytes. There was a significant decline in the activities of leucocyte GSH-px, GSSG-R and SOD in the post-patent period; whereas arginase activity rose significantly following the patent period of anaplasmosis. The activity of erythrocyte SOD declined in the post-patent stage. The infection also caused a decline in red cell GSH (P less than 0.05). The results suggest that the glutathione oxidant defence system of peripheral blood cells is significantly influenced by the Anaplasma infection.

Anaplasmosis↗

Alterations of host defence system after sleep deprivation are followed by impaired mood and psychosocial functioning.

In healthy humans, sleep deprivation (SD) has consistently been demonstrated to impair different parameters of the host defence system and of psychosocial functioning. However, the individual timing of these alterations and their possible association have remained unknown so far. We therefore investigated functional measures of the individual host defence system as well as of subjective well-being and psychosocial performance in 10 healthy male adults before and after SD, as well as after recovery sleep. In detail, we examined the number of leukocytes, granulocytes, monocytes, lymphocytes, B cells, T cells, T helper and cytotoxic T cells, natural killer (NK) cells as well as the interleukin-1 beta (IL-1 beta) release from platelets after serotonin (5-HT) stimulation. Mood and psychosocial performance (excitement, energy, ability to work and timidity) were measured by visual analogue scales. Taken together, SD induced a deterioration of both mood and ability to work, which was most prominent in the evening after SD, while the maximal alterations of the host defence system could be found twelve hours earlier, i.e., already in the morning following SD. Our findings therefore suggest an SD-induced alteration of these psychoimmune response patterns in healthy humans preceding deterioration of mood and psychosocial functioning.

Adult↗

Chemical properties of N-chlorotaurine sodium, a key compound in the human defence system.

N-chlorotaurine (NCT) is known to play an important role in the human defence system. The already proved utility of the sodium salt as a disinfectant in human medicine suggested a thorough investigation of its chemical properties. Chlorine transfer to N-H groups (transhalogenation) and oxidation of thio and aromatic compounds represent its main reactions. Auto-chlorination causes disproportionation forming N, N-dichlorotaurine (NDCT) with K(d) = [NDCT][taurine]/f(a)[NCT]2aH+ = (4.5 +/- 0.8) x 10(6), while the reaction with ammonium releasing NH2Cl is characterised by K(NHCl2) = [NH2Cl][taurine]/[NCT][NH4+]f(a)2 = 0.02 +/- 0.004. The verified unique stability and low level reactivity of NCT are considered essential for its function in the mammalian defence system and its practical applicability, which manifests itself in an optimal compromise between microbicidal activity and toxicity.

Disinfectants↗

In vitro interactions of thallium with components of the glutathione-dependent antioxidant defence system.

We investigated the hypothesis that thallium (Tl) interactions with the glutathione-dependent antioxidant defence system could contribute to the oxidative stress associated with Tl toxicity. Working in vitro with reduced glutathione (GSH), glutathione reductase (GR) or glutathione peroxidase (GPx) in solution, we studied the effects of Tl+ and Tl3+ (1-25 microM) on: (a) the amount of free GSH, investigating whether the metal binds to GSH and/or oxidizes it; (b) the activity of the enzyme GR, that catalyzes GSH regeneration; and (c) the enzyme GPx, that reduces hydroperoxide at expense of GSH oxidation. We found that, while Tl+ had no effect on GSH concentration, Tl3+ oxidized it. Both cations inhibited the reduction of GSSG by GR and the diaphorase activity of this enzyme. In addition, Tl3+ per se oxidized NADPH, the cofactor of GR. The effects of Tl on GPx activity depended on the metal charge: Tl+ inhibited GPx when cumene hydroperoxide (CuOOH) was the substrate, while Tl(3+)-mediated GPx inhibition occurred with both substrates. The present results show that Tl interacts with all the components of GSH/GSSG antioxidant defence system. Alterations of this protective pathway could be partially responsible for the oxidative stress associated with Tl toxicity.

Antioxidants↗

Physical activity, aerobic capacity and selected markers of oxidative stress and the anti-oxidant defence system in healthy active elderly men.

The relationship of oxidative stress and the anti-oxidant defence system to maximal oxygen consumption (VO2max) and habitual physical activity was assessed in 26 elderly men (71.0 +/- 4.2 years) and compared to that of 12 young men (22.1 +/- 5.1 years). Physical activity was assessed by a questionnaire. Malondialdehyde (MDA), plasma total anti-oxidant status (TAS), the levels of red blood cell (RBC) superoxide dismutase (SOD) and glutathione peroxidase (GPX), as well as serum GPX activities were determined under resting conditions. The older and young men had similar TAS and RBC SOD, while MDA, RBC GPX and plasma GPX were higher, and RBC SOD/GPX ratio was significantly lower in the older men. Neither MDA nor anti-oxidants were associated with any of the physical activity/aerobic capacity measures in the elderly men. We conclude that in healthy elderly men with a good nutritional status, indicators of the anti-oxidant defence system are not lower in comparison with young men. Increased RBC and plasma GPX coupled with a high level of lipid peroxidation marker may indicate an adaptation of anti-oxidant defences to sustained oxidative stress. Furthermore, the results of the present study suggest that the level of habitual physical activity and aerobic capacity have no major influence on the resting balance between radical generation and blood anti-oxidant potential in healthy older men.

Adolescent↗

Behaviour of the anti-oxidant defence system and heme oxygenase-1 protein expression in fructose-hypertensive rats.

1. Addition of fructose to a rat diet for various periods of time leads to hypertension, hyperinsulinaemia and dyslipidaemia and provides a model for testing oxidative stress parameters in the animals. 2. In the present study, oxidative stress generation, the soluble and enzymatic defence system and heme oxygenase-1 (HO-1) protein expression were investigated in the heart, liver and kidney of rats fed fructose for a period of 1 or 8 months. 3. Compared with the control group, fructose-hypertensive rats showed increased in lipid peroxidation only in the heart after both 1 and 8 months of fructose treatment. Changes in the behaviour of the soluble and enzymatic defence system and HO-1 protein expression were different depending on the organ. Increased or unaltered activities of anti-oxidant enzymes were found in the liver and kidney, respectively. Induction of HO-1 prevented the generation of oxidative stress in the liver, where the activity of anti-oxidant defence enzymes was not reduced. Increased expression of HO-1 protein was not able to prevent the generation of oxidative stress in the heart, where fructose treatment diminished the activity of anti-oxidant enzymes. 4. The results of the present study demonstrate that upregulation of HO-1 may prevent the generation of oxidative stress only when the anti-oxidant defence system is still operative.

Animals↗

The oxidant defence system in water-buffaloes (Bubalus bubalis) experimentally infected with Anaplasma marginale.

The glutathione (GSH) -oxidant defence system protects the erythrocytes and leucocytes from oxidative damage. Leucocyte -superoxide dismutase (SOD), GSH-peroxidase (GSH-px), GSH-reductase (GR), GSH-S-transferase (GSH-S-t) and arginase were examined in samples from buffaloes infected with Anaplasma marginale. All the enzymes, except arginase, were also studied in the red cell haemolysates from these animals. GSH-S-t, GSH- and glutathione-reductase (GR) levels in leucocytes decreased in infected animals suggesting a decline in the efficiency of the GSH-oxidant defence system. SOD levels increased but there was no change in leucocyte-arginase activity due to infection. Infection caused no significant changes in red cell SOD, GSH-px, GR and GSH. However, GSH-S-t significantly decreased (P less than 0.05).

Anaplasmosis↗

Experimentally induced hypo- and hyper-thyroidism influence on the antioxidant defence system in adult rat testis.

The objective of the present experiment was to study the effect of thyroid hormone on the antioxidant defence system of rat testis. Hypothyroidism induced in rats by 6-n propyl 2-thiouracil (PTU) treatment resulted in a reduction in body weight, seminal vesicle and ventral prostate gland. A further decrease in the weight of seminal vesicle was recorded following administration of T3 to hypothyroid rats. The oxidative stress parameters such as hydrogen peroxide and protein carbonyl content increased in the crude homogenate of testis of hypothyroid rats. T3 administration to hypothyroid rats resulted in no further change in the hydrogen peroxide level but the protein carbonyl content further elevated in the crude homogenate of testis. No significant change was observed in the endogenous lipid peroxidation level of the crude homogenate of testis whereas the FeSO4/ascorbic acid induced lipid peroxidation level decreased in hypothyroid rats and did not change further by T3 administration. Although the reduced glutathione level in the crude homogenate of testis did not change following hypothyroidism, oxidized glutathione level increased. The reduced and oxidized glutathione level decreased and increased, respectively following T3 administration to hypothyroid rats in comparison with PTU-treated rats. Activities of superoxide dismutase and catalase decreased in the post-mitochondrial fraction (PMF) of testis of hypothyroid rats. T3 injection to PTU-treated rats resulted in an elevation in the level of catalase activity only. The activity of glutathione peroxidase in the PMF of testis elevated in the hypothyroid rats and reduced following T3 treatment to hypothyroid rats. The results of the present study suggest that any alteration in the thyroid hormone level in the body affects the antioxidant defence system of testis of adult rats and, thereby, may affect the physiology of testis through oxidative stress.

Animals↗

Modulation of the activity of the internal defence system of the pond snail Lymnaea stagnalis by the avian schistosome Trichobilharzia ocellata.

Effects of infection with the avian schistosome Trichobilharzia ocellata on the activity of the internal defence system of the intermediate snail host Lymnaea stagnalis were studied, utilizing an in vitro phagocytosis assay for determining haemocyte activity. A distinction was made between plasma- and cell-associated effects. The period immediately after penetration of the parasite into the snail host (1.5-72 h post-exposure (p.e.)) was extensively studied. In addition, several time-points coinciding with the later-successive-stages of parasite development (2, 4, 6, 8 and 10 weeks p.e.) were investigated. Plasma-associated enhancement of defence activity was found between 1.5 and 6 h p.e., followed by plasma-associated suppression between 12 and 72 h p.e. A cell-associated activation was found between 1.5 and 6 h p.e. and also at 8 and 10 weeks p.e. How these effects on the defence system may be related to phenomena observed in infected snails at these time-points is discussed.

Analysis of Variance↗

Endogenous antioxidant defence system in rat liver following mercury chloride oral intoxication.

Mercury is a highly toxic metal which induces oxidative stress. Superoxide dismutases, catalase, and glutathion peroxidase are proteins involved in the endogenous antioxidant defence system. In the present study rats were administered orally, by gavage, a single daily dose of HgCl2 for three consecutive days. In order to find a relation between the proteins involved in the antioxidant defence and mercury intoxication, parameters of liver injury, redox state of the cells, as well as intracellular protein levels and enzyme activities of Mn-dependent superoxide dismutase (MnSOD), Cu-Zn-dependent superoxide dismutase (CuZnSOD), catalase, and glutathione peroxidase (GPx) were assayed both in blood and in liver homogenates. HgCl2 at the doses of 0.1 mg/kg produced liver damage which that was detected by a slight increase in serum alanine aminotransferase and gamma glutamyl transferase. Hepatic GSH/GSSG ratio was assayed as a parameter of oxidative stress and a significant decrease was detected, as well as significant increases in enzyme activities and protein levels of hepatic antioxidant defence systems. Changes in both MnSOD and CuZnSOD were parallel to those of liver injury and oxidative stress, while the changes detected in catalase and GPx activities were progressively increased along with the mercury intoxication. Other enzyme activities related to the glutathione redox cycle, such as glutathione reductase (GR) and glucose-6-phosphate dehydrogenase (G6PDH), also increased progressively. We conclude that against low doses of mercury that produce a slight oxidative stress and liver injury, the response of the liver was to induce the synthesis and activity of the enzymes involved in the endogenous antioxidant system. The activities of all the enzymes assayed showed a rapidly induced coordinated response.

Administration, Oral↗

Effect of Nigella sativa on glucose concentration, lipid peroxidation, anti-oxidant defence system and liver damage in experimentally-induced diabetic rabbits.

This study was carried out to investigate whether Nigella sativa could decrease the lipid peroxidation, increase the anti-oxidant defence system and also prevent the lipid-peroxidation-induced liver damage in experimentally induced diabetic rabbits. Fifteen New Zealand male rabbits were divided into three experimental groups: control, diabetic and diabetic and N. sativa-treated. The diabetes mellitus (DMI) was induced in the rabbits using 150 mg/kg of 10% alloxan. The diabetic + N. sativa-treated group was given extract of N. sativa seeds orally every day for 2 months after induction of DM. At the end of the 2-month experiment, blood samples were collected to measure malondialdehyde (MDA), glutathione (GSH), ceruloplasmin and glucose concentration, and livers were harvested for histopathological analysis. Treatment with N. sativa decreased the elevated glucose and MDA concentrations, increased the lowered GSH and ceruloplasmin concentrations, and prevented lipid-peroxidation-induced liver damage in diabetic rabbits. It was concluded that N. sativa might be used in diabetic patients to prevent lipid peroxidation, increase anti-oxidant defence system activity and also prevent liver damage.

Animals↗