Protective effect of light emitting diode phototherapy on fluorescent light induced retinal damage in Wistar strain albino rats.

BACKGROUND: Artificial light at night alters retinal physiology. Several studies have shown that light emitting diode phototherapy protects the retina from the damaging effects of acute light exposure. OBJECTIVE: The aim of this study has been to elucidate the protective effects of 670 nm LED light on retinal damage induced by chronic fluorescent light in Wistar rats. METHODS: Male Wistar albino rats were divided into four groups: group 1 were control (CL), group 2, 3 and 4 were exposed to fluorescent light (FL), LED preexposure+fluorescent light exposure (LL) and only LED light exposure (OL) respectively. All animals were maintained in their specific exposure regime for 30 days. Fluorescent light of 1800 lx was exposed between 8 pm to 8 am. Rats were exposed to therapeutic LED light of 670 nm of 9 J/cm2 at 25 mW/cm2 for 6 min duration. Histopathological changes in the retina were studied. RESULTS: Animals of the FL group showed a significant reduction in the outer nuclear layer thickness and cell count in addition to the total thickness of the retina. LL group which were exposed to 670 nm LED prior to exposure to fluorescent light showed a significant decrease in the degree of damage. CONCLUSIONS: 670 nm LED light preexposure is protective to retinal cells against fluorescent light-induced damage.

Second digit and fourth digit ratio--an adjunct tool to predict obstructive sleep apnea.

Obstructive sleep apnea (OSA) is a sleep related breathing disorder associated with high morbidity and mortality. Digit ratio (2D:4D) a sexually dimorphic trait is a putative indicator of prenatal testosterone exposure and adult testosterone level. Present study aimed at investigating the correlation between 2D:4D ratio and OSA based on the study conducted on 290 volunteered participants of both the sexes in the age range of 20-45 years. A significant negative correlation was observed for 2D:4D with OSA related parameters specifically Berlin score, Epworth score and certain key anthropometric measurements, neck circumference (NC) and waist-hip ratio (WHR). The study thus showed that lower 2D:4D ratio, increases risk of developing OSA and hence it can be used as an adjunct tool in the prediction of OSA.

Changes in maternal lipid peroxidation before and immediately after delivery.

Oxidative damage has been implicated in pathogenesis of many diseases. It is known that various kinds of stresses accelerate the production of free radicals. As pregnancy being a physiological state accompanied by a high energy demand of many bodily functions and an increased oxygen requirement, increased level of oxidative stress would be expected. The present study was to elucidate the degree of oxidative stress during labour and immediately after delivery. Twenty healthy pregnant women and age matched and 20 healthy non-pregnant women were selected as subjects for this longitudinal study. Plasma malondialdehyde concentration was estimated as thiobarbituric acid reacting substances. A significant (p < 0.01) increase in plasma malondialdehyde concentration was noted in pregnant women during labour than in the non-pregnant women. Plasma malondialdehyde concentration was noted to increase with the progression and duration of labour to immediately following delivery. Labour being stressful state results in oxidative stress, which increased with increase in duration and progression of the labour till immediately following delivery.

Effect of REM sleep deprivation on the antioxidant status in the brain of Wistar rats.

BACKGROUND: Rapid eye movement [REM] sleep deprivation is a stressor. It results in a predictable syndrome of physiological changes in rats. It has been proposed that reactive oxygen species and the resulting oxidative stress may be responsible for some of the effects of sleep deprivation. PURPOSE: The present study was undertaken to investigate the reversible nature of the effects of 96 hours of REM sleep deprivation on lipid peroxidation and total reduced glutathione level in the hypothalamus, midbrain and hindbrain of Wistar strain rats. METHODS: The rats were deprived of REM sleep using the inverted flowerpot technique. All the animals were maintained in standard animal house condition with 12-h light and 12-h dark cycles. At the end of the stipulated time Jugular venous blood sample of 2 ml was collected under mild ether anesthesia for the assay of stress index, plasma corticosterone. Lipid peroxidation using thiobarbituric acid, total reduced glutathione using DTNB (GSH) were assayed in the brain regions dissected out. RESULTS: This study showed that 96 hours of REM sleep deprivation results in increased lipid peroxidation and reduction in total reduced glutathione level in the discrete regions of brain studied. However following restorative sleep for 24 hours all the changes reverts back to base line value. This study shows that oxidative stress produced by 96 hours of REM sleep deprivation is reversible. CONCLUSION: From this study it is clear that, REM sleep deprivation is a potent oxidative stressor. This could probably play a role in the behavioral and performance alteration seen in both experimental animals as well as humans following REM sleep deprivation. Further investigations in this line are needed to highlight the importance of REM sleep.

Effect of alpha-ketoglutarate on neurobehavioral, neurochemical and oxidative changes caused by sub-chronic cyanide poisoning in rats.

Recent studies revealed that alpha-ketoglutarate (A-KG) alone or with sodium thiosulfate (STS) provide significant protection against acute and sub-acute cyanide poisoning in rodents. This study addresses the protective effect of A-KG and/or STS in sub-chronic (90 days) cyanide poisoning. Wistar rats were divided into seven groups (n = 10): Control animals, potassium cyanide (KCN) A-KG, STS, KCN + A-KG, KCN + STS and KCN + A-KG + STS. Spontaneous motor activity and motor coordination were recorded every 15th day. Lipid peroxidation (LPO), reduced glutathione (GSH), glutathione peroxidase (GPx), superoxide dismutase (SOD) and catalase (CAT) in blood, brain, liver and kidney, and glutamate, aspartate and dopamine in discrete regions of brain were measured following 90 days exposure. Cyanide significantly decreased motor coordination, accompanied by increase in LPO (blood, brain and liver) and dopamine (corpus striatum and cerebral cortex) levels, and depletion in GSH (blood, brain and liver), GPx (brain and liver), SOD (brain and liver), and CAT (blood and brain) levels. Although treatment of A-KG and STS alone significantly blunted the toxicity of KCN, concomitant use of both afforded the maximum protection. This study shows a promising role of A-KG and STS as treatment regime for long term cyanide exposure.

Behavioral analysis after sciatic nerve compression in albino rats.

BACKGROUND: Walking track analysis which has been widely used to examine the recovery of gait functions in rats with sciatic nerve injury. PURPOSE: The present study was aimed to objectively analyze and quantify the degree of functional recovery in locomotor behavior of rats after inflicting sciatic nerve crush injury. METHODS: Wistar rats trained on various runways, viz., narrow beam, grid and staircase, were subsequently tested following sciatic nerve crush injury. RESULTS: Locomotor ability of injured rats on runways gradually recovered to the level that was not significantly different from their corresponding preoperative level by the sixth postoperative week. CONCLUSION: Conventional run ways can be objectively used for quantification of the level of recovery.

Protective effect of diltiazem on cyanide-induced neurotoxicity in Wistar strain rats.

Cyanide is a well-established poison known for its rapid lethal action and toxicity. The central nervous system is one of the main target sites for cyanide toxicity. Cyanide not only alters brain biogenic amine levels but also the intracellular calcium levels in the neuronal cells. In the present study the role of calcium channel blocker diltiazem (DIL) in cyanide induced biogenic amine changes was evaluated in the Wistar strain rats. The protective effect of diltiazem pretreatment and diltiazem treatment along with cyanide on the dopaminergic system and the serotonergic system in the corpus striatum were studied. Diltiazem pretreatment was found to prevent cyanide induced changes in both the amines in the corpus striatum. These results suggest that diltiazem may mitigate the harmful effects of cyanide by interfering with influx of calcium ions and release of the biogenic amines.

Calcium ions: its role in cyanide neurotoxicity.

Cyanide is a well-established poison known for its rapid lethal action and toxicity. The central nervous system is one of the main target sites for cyanide toxicity. Cyanide also alters the brain biogenic amine levels. In the present study the role of calcium ions in cyanide toxicity was evaluated using the calcium channel blocker diltaizem (DIL) in Wistar strain albino rats. This study showed that DIL pretreatment prevented cyanide induced changes in the dopaminergic and serotonergic system in the corpus striatum.

Free radical changes in methanol toxicity.

Role of free radicals in methanol toxicity was evaluated in methanol treated albino rats. Methanol intoxication increased lipid peroxidation and depleted the free radical scavenging enzyme systems. The free radical quenching effect of vitamin E protected the animals from methanol induced free radical damage.

Effect of chronic protein restriction on motor co-ordination and brain neurotransmitters in albino rats.

In this study we evaluated the motor co-ordination in Wistar strain albino rats that were maintained on a protein-restricted diet for a period of 1 year immediately after the weaning period, by substituting 75% of the normal diet with a carbohydrate-rich diet deficient in protein, for a period of 1 year immediately after the weaning period. This type of chronic protein restriction caused disturbances in motor co-ordination. It also caused a significant reduction in the basal levels of dopamine, norepinephrine, epinephrine and serotonin along with their metabolites homovanillic acid (HVA), vanillyl mandelic acid (VMA) and 5-hydroxy indoleacetic acid (5HIAA) and precursor L-dopa in the corpus striatum and cerebellum. Changes in these neurotransmitters could have caused altered co-ordination in the protein-restricted animals.

Effect of cassava consumption on open-field behavior and brain neurotransmitters in albino rats.

Diet exerts a critical influence on human biology and thus studies on the interrelationship of nutrition and behavior continues to be a major and important focus of research in the natural experimental sciences. Cassava is known to cause metabolic and neurological derangement on long-term consumption as a staple diet in the tropics. In this article we present the effects of cassava consumption on open-field behavior and catecholamine levels in the hypothalamus of albino rats. Cassava consumption for 30 days alters the emotional status of the rats, with changes in the basal neurotransmitter levels in the hypothalamus. The role of the cyanide (liberated from cassava) and protein deficiency (associated with cassava consumption) has been discussed.

Long-term ingestion of cassava (tapioca) does not produce diabetes or pancreatitis in the rat model.

Cassava (tapioca, manihot) is consumed as a staple food in some developing countries. The intake of cassava has been linked to several diseases including fibrocalculous pancreatic diabetes (tropical calcific pancreatitis). There are few long-term studies on the effect of cassava ingestion on the pancreas in animal models. This article reports on the long-term (up to 1 yr) effects of cassava in the rat model. We found that cassava did not produce diabetes in the rat even after a year of cassava feeding. There were transient changes in serum insulin and lipase levels, but the significance of these findings are not clear. There was no histopathological evidence of either acute or chronic pancreatitis, but there were changes of toxic hepatitis in the liver. In conclusion, chronic cassava ingestion up to a year does not lead to either diabetes or chronic pancreatitis in the rat model.

Effect of chronic cyanide intoxication on memory in albino rats.

Cyanide is a chemical widely used in industry, and is a major environmental pollutant. Its toxicity is caused by inhibition of cytochrome oxidase resulting in histotoxic hypoxia. The effect of sublethal doses of cyanide on memory and hippocampal neurotransmitters was studied in male Wistar strain albino rats. Cyanide reduced the memory along with reduction in the levels of dopamine and 5-hydroxytryptamine in the hippocampus. Pre-existing malnutrition in the animals exaggerated these effects.

Neurochemical and behavioural correlates in cassava-induced neurotoxicity in rats.

Chronic cyanide intoxication from cassava has been implicated as the cause for a degenerative neuropathy known widely as tropical ataxic neuropathy. An attempt has been made in this study to identify the specific cause for neuropathy caused by cassava using Wistar strain albino rats as the experimental animal model. The results of cassava fed animals were compared with control animals, animals given cyanide, malnourished animals and malnourished animals fed cyanide, to identify the causative factors. This study revealed that though the behavioural pattern in motor coordination of the cassava fed animals was similar to the other groups studied, the neurochemical basis for the observed behavioural pattern was unique for cassava. Hence the neurotoxicity of cassava could be attributed to unmetabolized linamarin, more than its nutritional status and/or cyanide toxicity.

Effect of Cassava on motor co-ordination and neurotransmitter level in the albino rat.

The root of Cassava, a tropical plant, is consumed in the tropics and has been attributed as the cause for various tropical neuropathies. This study aims to discover the neurotoxic effects of chronic cassava consumption of Indian origin and the effect of malnutrition. The assessment is based on the motor co-ordination and brain neurotransmitters in rats. Cassava consumption reduced the motor co-ordination, but the changes in neurotransmitter levels due to cassava consumption (except for 5HT in corpus striatum) was identical with malnutrition-induced changes, indicating that the toxicity of chronic cassava consumption (of Indian origin) is mainly due to the associated protein calorie malnutrition (PCM).

Activated charcoal--an antidote to methyl alcohol poisoning.

Every year a considerable number of people die due to methly alcohol poisoning, in which most of them die even before they are given proper treatment. This report gives a simple and cheap first aid measure to those affected by methanol poisoning by the administration of activated charcoal. This study has shown that the mortality of methanol recipient rats have significantly reduced by the administration of activated charcoal.