Biomedical subjects

Bimla Nehru

Publications and source records attributed to Bimla Nehru.

5 recordsLinked to original sources

PubMed2006

Evidence for centrophenoxine as a protective drug in aluminium induced behavioral and biochemical alteration in rat brain.

Potential use of various nootropic drugs have been a burning area of research on account of various physical and chemical insult in brain under different toxicological conditions. One of the nootropic drug centrophenoxine, also known as an anti-aging drug has been exploited in the present experiment under aluminium toxic conditions. Aluminium was administered by oral gavage at a dose level of 100 mg/Kg x b x wt/day for a period of six weeks. To elucidate the region specific response, study was carried out in two different regions of brain namely cerebrum and cerebellum. Following aluminium exposure, a significant decrease in the activities of enzymes namely Hexokinase, Lactate dehydrogenase, Succinate dehydrogenase, Mg(2+) dependent ATPase was observed in both the regions. Moreover, the activity of acetylcholinesterase was also reported to be significantly decreased. Post-treatment with centrophenoxine was able to restore the altered enzyme activities and the effect was observed in both the regions of brain although the activity of lactate dehydrogenase and acetylcholinesterase did not register significant increase in the cerebellum region. Further, centrophenoxine was able to improve the altered short-term memory and cognitive performance resulted from aluminium exposure. From the present study, it can be concluded that centrophenoxine has a potential and can be exploited in other toxicological conditions also.

Acetylcholinesterase↗

PubMed2006

Reversal of an aluminium induced alteration in redox status in different regions of rat brain by administration of centrophenoxine.

Aluminium is one of the most studied neurotoxin, and its effects on nervous system are both structural and functional, involving various regions of brain. Aluminium toxicity is known to have multiple mechanisms of action in the central nervous system. Affinity of aluminium for thiol substrates is considered a possible molecular mechanism involved in aluminium neurotoxicity. The reduced glutathione (GSH) is especially important for cellular defence against aluminium toxicity. This study pertains to the modulatory action of centrophenoxine on GSH status in aluminium exposed different brain regions of the female rats. Aluminium was administered orally at a dose of 40 mg/Kg x b x wt x /day for a period of eight weeks whereas, centrophenoxine was administered intraperitoneally at a dose of 100 mg/Kg x b x wt x /day for a period of six weeks. The study was carried out in different regions of brain namely cerebrum, cerebellum, medulla oblongata and hypothalamus. Animals exposed to aluminum, registered a significant decrease in the levels of reduced glutathione, and oxidized glutathione as well as in the activity of glutathione reductase in all the different regions studied when compared to normal control animals. Post-treatment with centrophenoxine, showed a significant improvement in the thiol levels in different regions. Centrophenoxine when administered alone also had a profound effect on the levels of reduced glutathione as well as on the activity of glutathione reductase. From the present results, it can be stated that centrophenoxine administration, as a thiol-antioxidant, arrests the aluminium induced cellular damage by improving the thiol status in brain regions.

Aluminum↗

PubMed2005

Oxidative damage following chronic aluminium exposure in adult and pup rat brains.

Aluminium is known to cause neurotoxic effects. In the past few years there has been an upsurge of interest in aluminium exposure through diet and environment, which might impair the development of mammals. The present in vivo study was designed to investigate the potential of aluminium to participate in either antioxidant or pro-oxidant processes in both developed and developing rat brain. Markers of oxidative stress were determined in rat brains exposed to AlCl3 (100 mg/kg body weight) for 8 weeks. The aluminium dose was given to adult rats for 8 weeks and in another group, exposure of aluminium for 60 days was done postnatally, 21 days to the feeding mother (lactation period) and 39 days to the rat pups. The results showed a statistically significant (p<or=0.01) increase in lipid peroxidation (LPx) as measured by production of malondialdehyde in both cerebrum and cerebellum of pup brains. A significant increase (p<or=0.001) in LPx was also observed in the adult group. Furthermore, aluminium exposure resulted in a significant decrease in superoxide dismutase and catalase activity in both regions of the brain of developing and developed rat brain. Thus the results of the present study suggest that in rats, aluminium (100 mg/kg body weight) has a pro-oxidant effect and thus acts as a neurotoxin.

Aluminum↗

PubMed2005

Modulatory effects of centrophenoxine on different regions of ageing rat brain.

The debilitating consequences of age-related brain deterioration are widespread and extremely costly in terms of quality of life and longevity. Free radical induced damage is thought to be responsible, at least in part, for the degenerative effects of aging. This may be largely due to high-energy requirements, high oxygen consumption, high tissue concentration of iron and low of antioxidant enzymes in brain. Therefore, supplementing an external source of free radical scavenger would greatly benefit in ameliorating the free radical damage which may thus be beneficial in aging. In the present study, an important nootropic agent Centrophenoxine, which has an easy access to brain, has been administered to aged animals (16 months old). Rats aged 6 months (young group) and 16 months old (old group) were chosen for the study. Both groups were administered Centrophenoxine (dissolved in physiological saline) intraperitoneally once a day for 6 weeks. Our study indicates an increased activity of Catalase, Superoxide Dismutase, Glutathione reductase, as well as an increase in the reduced, oxidized, and total glutathione content thus resulting in an altered redox state. A substantial increase in the malondialdehyde content was also reported as a result of aging. Whereas, following Centrophenoxine administration (100 mg/kg body weight/day, injected i.p) alterations in the activities of Superoxide dismutase, Glutathione reductase as well as in the reduced and oxidized glutathione content was reported in aged rat brain. Lipid peroxidation was also reported to be significantly decreased in aged animals after Centrophenoxine supplementation for 6 weeks. The use of an extraneous antioxidant substance may prove beneficial in combating the conditions of oxidative stress in ageing brain.

Aging↗

PubMed2003

Relationship between lead-induced biochemical and behavioral changes with trace element concentrations in rat brain.

Lead has an obvious potential to disturb learning ability, adaptive responses, and other aspects of behavior and even personality in those who may appear healthy according to conventional medical criteria. These disturbances are shown to be associated with alterations in ionic, cholinergic, and dopaminergic neurotransmission in the central nervous system (CNS). The present experiment was designed to study the neurotoxic consequences of lead exposure on neurotransmitters like dopamine, serotonin, norepinephrine, and activity of acetylcholinestrase, as well as some ions like zinc, calcium, sodium, and potassium. The locomotory functions along with cognitive functions and memory loss were also studied at various dose levels. Lead was administrated orally in doses of 10 mg/kg, 50 mg/kg, and 200 mg/kg for a period of 12 wk and the study was done at the end of exposure. A dose-dependent decrease in the concentration of sodium, potassium, and zinc was observed; there was increase in the concentrations of lead and calcium. The most significant change noted was the decrease in activity of the acetylcholinestrase and other neurotransmitters. Lead exposure affected the locomotor and cognitive functions. Short-term memory remained unchanged at all lead exposure doses.

Acetylcholinesterase↗