Biomedical subjects

P K Banerjee

Publications and source records attributed to P K Banerjee.

At least 19 recordsLinked to original sources

PubMed2006

Adaptogenic and safety evaluation of seabuckthorn (Hippophae rhamnoides) leaf extract: a dose dependent study.

The effects of seabuckthorn (Hippophae rhamnoides L., Elaeagnaceae), leaf aqueous extract were examined in rats for its adaptogenic activity and toxicity. Dose dependent adaptogenic study of extract was carried out at different doses administered orally, 30min prior to cold (5 degrees C)-hypoxia (428mmHg)-restraint (C-H-R) exposure. After sub-acute toxicity studies on 10 and 20 times doses of maximal effective dose administered for 14 days (single oral dose of 1g/kg and 2g/kg once daily) and maximal effective dose administered for 30 days (single oral dose of 100mg/kg once daily), biochemical and hematological parameters were studied in the serum and blood. The maximal effective adaptogenic dose of the extract was 100mg/kg body weight. No significant changes were observed in organ weight/body weight ratios, of any vital organ studied (except liver and kidney in 1g/kg and 2g/kg body weight doses, respectively), and biochemical and hematological parameters of the sub-acute drug treated animals in comparison to control rats. In acute toxicity study LD(50) of the extract was observed to be >10g/kg when given orally. These results indicate that seabuckthorn leaf aqueous extract possess potent adaptogenic activity with no toxicity even after sub-acute (30 days) maximal effective dose administration.

Animals↗

PubMed2006

Studies on immunogenicity and protective efficacy of DnaJ of Salmonella Typhi against lethal infection by Salmonella Typhimurium in mice.

In the present study DnaJ (HSP40) of Salmonella enterica serovar Typhi has been evaluated for its immunogenicity and efficacy in protecting mice against lethal challenge by S. enterica serovar Typhimurium infection. DnaJ was amplified by PCR of the genomic DNA of S. Typhi and subsequently cloned in pQE-30 expression vector. The protein was induced by IPTG and purified using Ni-NTA chromatography under denaturing conditions. After refolding in vitro the immune response was evaluated by injecting 40 microg DnaJ protein/mouse i.p. on 0th, 7th and 28th day. The results showed a significant increase in antibody titre and lymphocyte proliferation in animals immunised with DnaJ as compared to control. Further there was an appreciable increase in IL-2, IL-4, IFN-gamma production in lymphocytes isolated from immunised mice as compared to control. In this limited study, immunisation of mice with DnaJ was found to provide 70% protection against lethal challenge by S. Typhimurium indicating the possible use of DnaJ as vaccine candidate against typhoid.

Animals↗

PubMed2006

Flavonoids protect U-937 macrophages against tert-butylhydroperoxide induced oxidative injury.

The study was carried out to determine the relative efficacies of polyphenolic flavonoids, quercetin, catechin and epicatechin against tert-BOOH induced oxidative stress in human macrophage, U-937 cell line. Exposure of the cells to tert-BOOH oxidative stress resulted in a significant increase in cytotoxicity and reactive oxygen species (ROS) generation. Further, a significant decrease in mitochondrial membrane potential and increase in lipid peroxidation and DNA damage was observed in cells exposed to tert-BOOH. Pretreatment of cells with quercetin, catechin and epicatechin significantly inhibited tert-BOOH induced cytotoxicity by inhibiting ROS generation. The flavonoids inhibited DNA damage induced by tert-BOOH and preserved the mitochondrial transmembrane potential significantly. Epicatechin and catechin were found to be more efficient than quercetin in inhibiting tert-BOOH induced cellular damage.

Antioxidants↗

PubMed2006

Quercetin protects C6 glial cells from oxidative stress induced by tertiary-butylhydroperoxide.

The anti-oxidant and cyto-protective activity of quercetin against tertiary-butylhydroperoxide (t-BOOH) induced oxidative stress on C6 glial cells is reported. Exposure of the cells to t-BOOH resulted in a significant increase in cytotoxicity, reactive oxygen species (ROS) generation and lipid peroxidation. There was a significant increase in DNA strand breaks and fall in reduced GSH levels in cells exposed to t-BOOH. A significant increase in calcium ion influx was noticed in cells exposed to t-BOOH. Pre-treatment of cells with quercetin, vitamin C (vit C), Trolox, and deferoxamine (DFO) significantly inhibited t-BOOH induced cytotoxicity and ROS generation. Pretreatment of cells with quercetin, Trolox and DFO inhibited the DNA damage, maintained higher GSH levels and prevented calcium influx significantly. Although vit C protected the cells from cytotoxicity induced by t-BOOH, the intracellular Ca(2+) levels were significantly higher than the control cells. However, anti-oxidants like butylated hydroxy toluene (BHT), vitamin E (vit E), N-acetyl cysteine (NAC) did not have significant cytoprotection against t-BOOH induced oxidative injury in C6 glial cells.

Cell Survival↗

PubMed2005

Comparative cytoprotective activity of vitamin C, E and beta-carotene against chromium induced oxidative stress in murine macrophages.

The present study reports the cytoprotective efficacy of vitamin C, E and beta-carotene against chromium (VI) induced oxidative stress in murine macrophages. Addition of chromium (VI) resulted in enhanced cytotoxicity as revealed by fall in neutral red uptake and increase in LDH release compared to control cells. Further there was an appreciable increase in apoptosis, ROS production and fall in reduced glutathione (GSH), glutathione peroxidase (GPx) and superoxide dismutase (SOD) activities. Chromium also inhibited macrophage proliferation and phagocytic activity. Addition of vitamin C but not vitamin E and beta-carotene inhibited chromium induced cytotoxicity, ROS generation and apoptosis. Vitamin C significantly inhibited NO production, enhanced macrophage proliferation and phagocytic activity while vitamin E and beta-carotene had marginal effect.

Animals↗

PubMed2005

Neuroprotective effect of N-acetyl cysteine on hypoxia-induced oxidative stress in primary hippocampal culture.

Hippocampus has received a considerable attention in the recent past due to its role in a number of important functions such as learning and memory. The effect of hypoxia on neuronal cell injury especially on hippocampal cells is not well known. The aim of the present study was to characterize the biochemical changes in primary cultured hippocampal neurons during hypoxic exposure and the protective effect of N-acetyl cysteine on hypoxia-induced cytotoxicity. The hippocampal culture grown in 24-well plates was exposed to hypoxia for 3 h in a dessicator in 95% N(2), 5% CO(2) atmosphere at 37 degrees C. Later, the cells were allowed to recover for 1 h under normoxia. It was observed that there is an appreciable increase in cytotoxicity in cells exposed to hypoxia. Further, there was a significant decrease in mitochondrial membrane potential and appreciable increase in reactive oxygen species and single-strand DNA breaks in cells exposed to hypoxia compared to control. There is a significant fall in glutathione peroxidase, glutathione reductase, reduced glutathione levels, and nitric oxide in the cells exposed to hypoxia. Significant elevation in the intracellular calcium level in the cells on exposure to hypoxia was observed. Supplementation with NAC (50 microM) resulted in a significant cytoprotection, fall in ROS generation, and higher antioxidant levels similar to that of control cells. NAC also inhibited DNA strand breaks induced by hypoxia. The study indicates that NAC has significant neuroprotective activity during hypoxia in primary hippocampal culture.

Acetylcysteine↗

PubMed2005

Immunomodulatory effects of seabuckthorn (Hippophae rhamnoides L.) against chromium (VI) induced immunosuppression.

The present study reports the immunomodulatory effects of seabuckthorn (Hippophae rhamnoides L.) leaf extract on cellular and humoral immune response by studying delayed-type hypersensitivity response, IL-2, IL-4 and gamma-IFN levels and antibody titres in chromium-induced immunosuppressed animals. Oral feeding of chromium (30 mg/kg bw) significantly inhibited antibody production and S-RBC induced delayed-type hypersensitivity response. Administration of leaf extract (100 mg/kg bw) along with chromium significantly inhibited chromium-induced immunosuppression. To understand the immunomodulatory mechanism of leaf extract, in vitro studies were carried out using rat lymphocytes. Addition of chromium resulted in a significant decrease in lymphocyte size and increased ROS generation. The leaf extract of seabuckthorn significantly inhibited chromium-induced reactive oxygen species (ROS) generation and maintained the cell size identical to that of control cells. Chromium treatment markedly inhibited the mitochondrial transmembrane potential by larger lymphocytes in particular, while the leaf extract restored the same significantly. Chromium also inhibited significantly concanavalin A (ConA) induced IL-2, IL-4 and gamma-IFN production in rat lymphocytes. The leaf extract (100 microg/ml) alone stimulated IL-2 and gamma-IFN production even in the absence of ConA and also inhibited chromium-induced decline in IL-2 and gamma-IFN production but it did not change IL-4 production. These observations suggest that the leaf extract of seabuckthorn has significant immunomodulatory activity and specifically activates the cell-mediated immune response.

Animals↗

PubMed2005

Antioxidant activities of seabuckthorn (Hippophae rhamnoides) during hypoxia induced oxidative stress in glial cells.

The present study reports the cytoprotective and antioxidant properties of alcoholic leaf extract of seabuckthorn (SBT) against hypoxia induced oxidative stress in C-6 glioma cells. Exposure of cells to hypoxia for 12 h resulted in a significant increase in cytotoxicity and decrease in mitochondrial transmembrane potential compared to the controls. Further an appreciable increase in nitric oxide and reactive oxygen species (ROS) production was noted which in turn was responsible for fall in intracellular antioxidant levels and GSH/GSSG ratio. There was a significant increase in DNA damage during hypoxia as revealed by comet assay. Pretreatment of cells with alcoholic leaf extract of SBT at 200 mug/ml significantly inhibited cytotoxicity, ROS production and maintained antioxidant levels similar to that of control cells. Further, the leaf extract restored the mitochondrial integrity and prevented the DNA damage induced by hypoxia. These results indicate that the leaf extract of SBT has strong antioxidant and cytoprotective activity against hypoxia induced oxidative injury.

Antioxidants↗

PubMed2005

Cytoprotective and antioxidant activity of Rhodiola imbricata against tert-butyl hydroperoxide induced oxidative injury in U-937 human macrophages.

The present study reports cytoprotective and antioxidant activity of aqueous and alcoholic extracts of Rhodiola imbricata rhizome on tert-butyl hydroperoxide (tert-BHP) induced cytotoxicity in U-937 human macrophages. There was an increase in cytotoxicity and apoptosis significantly in the presence of tert-BHP over control cells. The tert-BHP induced cytotoxicity can be attributed to enhanced reactive oxygen species (ROS) production which in turn is responsible for fall in reduced glutathione (GSH) levels; further there was a significant decrease in mitochondrial potential and increase in apoptosis and DNA fragmentation. Both aqueous and alcoholic extracts of Rhodiola rhizome at a concentration of 250 microg/ml were found to inhibit tert-BHP induced free radical production, apoptosis and to restore the anti-oxidant levels to that of the control cells. The alcoholic extract of Rhodiola showed higher cytoprotective activities than aqueous extract. These observations suggest that the alcoholic and aqueous extracts of Rhodiola have marked cytoprotective and antioxidant activities.

Antioxidants↗

PubMed2005

Ghrelin and leptin levels of sojourners and acclimatized lowlanders at high altitude.

The circulatory levels of two appetite regulatory hormones i.e. leptin and ghrelin were estimated in sojourners and acclimatized subjects to investigate their possible role in high altitude (HA) induced anorexia. A group of 30 lowlanders who had never visited HA were inducted to a height of 3600 m by air and after 48 h they were further taken to an altitude of 4300 m by road. Blood samples were collected after 48 h stay at 3600 m and again after 48 h and 7 days of stay at 4300 m during 0700-0730 h. There was a decrease in energy intake (850 kcal/day) of sojourners, which resulted in loss of body weight by 2.12 kg at HA. At an altitude of 4300 m there was a significant increase in leptin over basal levels (54.9%, p < 0.001) at 48 h that persisted even after 7 days of stay at this altitude. Ghrelin levels of sojourners decreased by more than 30% in comparison to basal values at 48 h of ascent to HA. Leptin levels of acclimatized lowlanders were also higher in comparison with control group (acclimatized group 7.6 + 0.6 ng/ml vs. control 5.6 + 0.5 ng/ml, p < 0.01, n = 50).

Acclimatization↗

PubMed2005

Appetite regulatory peptides in Indian Antarctic expeditioners.

Antarctica presents an inhospitable environment due to extreme low temperature, high wind velocity, low humidity, snowstorms, long polar days and nights, high level of UV radiations, magnetic storms and increased ionisation along with social isolation and sexual deprivation. Acclimatisation to any new condition is associated with certain metabolic changes along with alteration in nutritional requirements. There are reports of increased food intake and gain in body weight during past Indian Antarctic expeditions. Therefore, the present study was undertaken with the aim to assess the changes in appetite regulatory peptides i.e. leptin and neuropeptide Y in relation to energy intake and expenditure of the Antarctic expeditioners. The study was conducted in three phases viz. Phase I at Goa (basal), Phase II 48 h after reaching Antarctica and Phase III after one month of stay at Antarctica. Energy and nutrient intake were analysed from the duplicate plate samples of the expeditioners. Energy expenditure was computed using 24 h activity records for 7 days. Blood samples were collected in each phase for biochemical estimations. After reaching Antarctica, the expeditioners were active and the total energy expenditure (mean +/- SEM, n = 10) was found to be 3120 +/- 474 kcal/day. The actual energy intake was found to be 3911 +/- 310 kcal/day. This indicates that the Antarctic expeditioners had very active life and weight gain during expedition could be due to positive energy balance. After 48 h of stay at Antarctica plasma leptin levels (mean +/- SEM, n = 22) decreased from normal basal values 5.66 (+/- 0.59) ng/ml (Phase I) to 4.40 (+/- 0.37) ng/ml (Phase II), even though there was an increase in body fat. Increased level of plasma leptin was observed in Phase III as compared to phase I and II. Concomitantly there was increase in plasma neuropeptide Y levels from 0.303 (+/- 0.004) ng/ml to 1.211 (+/- 0. 27) ng/ml (p < 0.001) in Phase II and decrease in Phase III. The decrease in plasma leptin levels and increase in neuropeptide Y levels in Phase II may be responsible for increase in appetite and gain in body weight at Antarctica.

Adult↗

PubMed2005

Effect of hypobaric hypoxia on visual evoked potential at high altitude.

The effect of hypobaric hypoxia on visual evoked potential (VEP) was studied in 27 male volunteers at sea level (SL), during the 1st and 3rd weeks of their stay at high altitude (HA) of 3,500 m and in the 1st week of their return to the sea level (RSL). Exposure to high altitude (HA) led to significant changes in VEP. The N1 wave latency of both right and left eye was significantly increased (P<0.05) during 3rd week of stay at the altitude which persisted even after the return to the sea level. The latency of P1 wave of both right and left eye was higher in 3rd week at high altitude but not significant statistically. But the delay in P1 latency persisted in 1st week of their return to sea level which was significant (p<0.05) statistically as compared to sea level. The latency of N2 wave was significantly decreased (P<0.05) during the 1st week of stay at HA and returned back to basal value in the 3rd week of stay at HA in both right and left eye. However, the changes observed in NPN complex in terms of wave latencies were within the physiological limits. The amplitude of wave N1-P1 of both the right and left eye did not show any change. The changes observed reflect the process of acclimatisation to 3500m high altitude.

Adult↗

PubMed2004

Effect of chronic hypobaric hypoxia on components of the human event related potential.

BACKGROUND & OBJECTIVES: Induction to high altitude (HA) leads to deterioration in cognitive functions. The event related potentials (ERPs) like P300 are reported to be affected by hypoxia and bring about impairments in cognitive performance. The aim of the study was to investigate the effect of hypobaric hypoxia on event related potentials at two different altitudes i.e., 3200 m (HA I) and 4300 m (HA II) in ascending order to see how ERPs change with increasing altitude. METHODS: The study was carried out on 20 healthy male volunteers at sea level (SL) and thereafter at high altitude (HA) in Eastern Himalayas and on return to sea level (RSL). The P300 was recorded by using standard auditory odd ball paradigm with compact -4 (Nicolet, USA). RESULTS: The N1, N2 and P2 latencies were not significantly affected at HA I and HA II in comparison with SL indicating no effect of hypobaric hypoxia on sensory conduction. However, at HA II, most of the subjects showed an increase in latency of P3 component reflecting sensory discrimination and delay in evaluation process at 4300 m. At HA I, only 10 out of 20 subjects showed an increase in P3 wave latency and 3 did not show any change in N2-P3 components. INTERPRETATION & CONCLUSION: The results of the present study showed an increase in P300 wave latency at 3200 and 4300 m of high altitude. The observations suggest that hypoxia causes slowing of the signal processing at 4300 m, and magnitudes of the effects are altitude dependent with higher level of decline observed with increasing altitude.

Adult↗

PubMed2004

Effect of high altitude on human auditory brainstem responses.

The effect of hypobaric hypoxia on Brain Stem Auditory evoked potentials (BAERs) were studied. BAERs were recorded in 30 volunteers at sea level (SL) and then at high altitude (HA) of 3200 m (HA I) and 4300 m (HA II) in Eastern Himalayas and on return to sea level (RSL). The BAERs were recorded using Nicolet Compact - 4 (USA) in response to monaural auditory stimuli consisting of clicks of 100 ps square pulse at a rate of 15/sec. The BAERs were recorded on day 4 of their stay at 3200 m and 4300 m respectively. Findings indicated an increase in absolute peak latencies of wave V at 3200 m, which was statistically significant. On further ascent to 4300 m there was an increase in absolute peak latencies of wave I and III indicating delay in sensory conduction at the medullo-pontine auditory pathways.

Adult↗

PubMed2004

Changes in visual evoked potentials on acute induction to high altitude.

BACKGROUND & OBJECTIVES: Induction to high altitude leads to altered central nervous system (CNS) functions induced by hypobaric hypoxia. The sensory systems like visual and auditory systems are reported to be affected by hypoxia. The present study was undertaken to assess the effects of hypobaric hypoxia on visual evoked potentials (VEPs) at 3200 m and 4300 m. METHODS: The VEP of 30 human volunteers were recorded at sea level (SL) and then at high altitude (HA) of 3200 m (HA I) and 4300 m (HA II) in eastern Himalayas and on return to sea level (RSL). The absolute latencies and amplitude of positive and negative waves were recorded. RESULTS: High altitude of 3200 m did not alter the latency of major wave N1, P1 and N2 of the VEPs. At HA II (4300 m), there was a statistically significant increase (P < 0.01) in the latency of NI wave as compared to the SL value and HA I (3200 m) in both left and right eye. There was a slight increase in latenty of P1 wave in both left and right eye at HA II. INTERPRETATION & CONCLUSION: From these results it may be concluded that induction to HA causes increase in latency of N1 wave at 4300 m which is still within physiological limits. This increase in wave latency of N1 wave in both eyes may be due to synaptic delay and/or altered neuronal processing at HA.

Adult↗

PubMed2004

Auditory evoked functions in ground crew working in high noise environment of Mumbai airport.

The continuous exposure to the relatively high level of noise in the surroundings of an airport is likely to affect the central pathway of the auditory system as well as the cognitive functions of the people working in that environment. The Brainstem Auditory Evoked Responses (BAER), Mid Latency Response (MLR) and P300 response of the ground crew employees working in Mumbai airport were studied to evaluate the effects of continuous exposure to high level of noise of the surroundings of the airport on these responses. BAER, P300 and MLR were recorded by using a Nicolet Compact-4 (USA) instrument. Audiometry was also monitored with the help of GSI-16 Audiometer. There was a significant increase in the peak III latency of the BAER in the subjects exposed to noise compared to controls with no change in their P300 values. The exposed group showed hearing loss at different frequencies. The exposure to the high level of noise caused a considerable decline in the auditory conduction upto the level of the brainstem with no significant change in conduction in the midbrain, subcortical areas, auditory cortex and associated areas. There was also no significant change in cognitive function as measured by P300 response.

Adult↗

PubMed2003

High altitude hypoxia: an intricate interplay of oxygen responsive macroevents and micromolecules.

Physiological responses to high altitude hypoxia are complex and involve a range of mechanisms some of which occur within minutes of oxygen deprivation while others reset a cascade of biosynthetic and physiological programs within the cellular milieu. The O2 sensitive events occur at various organisational levels in the body: at the level of organism through an increase in alveolar ventilation involving interaction of chemoreceptors, the respiratory control centers in the medulla and the respiratory muscles and the lung/chest wall systems; at tissue level through the pulmonary vascular smooth muscle constriction and coronary and cerebral vessel vasodilation leading to optimized blood flow to tissues; at cellular level through release of neurotransmitters by the glomus cells of the carotid body, secretion of erythropoietin hormone by kidney and liver cells and release of vascular growth factors by parenchymal cells in many tissues; at molecular level there is expression/activation of an array of genes redirecting the metabolic and other cellular mechanisms to achieve enhanced cell survival under hypoxic environment. Transactivation of various oxygen responsive genes is regulated by the activation of various transcriptional factors which results in expression of genes in a highly coordinated manner. There is thus an intricate cascading interplay of biochemical pathways in response to hypoxia, which causes changes at the physiological and molecular levels. Added to this interplay is the possibility of genetic polymorphism and protein changes to adapt to environmental influences, which may allow a variability in the activity of the pathway. Our understanding of these interactions is growing and one may be close to the precise combination of genetic factors and protein factors that underlie the mechanism of what goes on under high altitude hypoxic stress and who will cope at high altitude.

Altitude↗

PubMed2003

Hypoxic ventilatory response changes of men and women 6 to 7 days after climbing from 2100 m to 4350 m altitude and after descent.

To test the hypothesis that the changes in hypoxic ventilatory response (HVR) of men and women mountaineers on induction to HA by trekking is not influenced by gender, isocapnic HVR as DeltaV(E)/DeltaSa(O2) was studied in eight men and eight women mountaineering trainees initially at 2100 m, then during 6 to 7 days of sojourn at 4350 m, and retested again on return to 2100 m. Results indicated that HVR at 2100 m increased significantly at 4350 m in both sexes, and the values reverted to baseline level within 4 to 5 days between leaving high altitude (4350 m) and restudy at 2100 m. No sex differences were observed at 2100- or at 4350-m altitude, indicating that men and women have a similar level of chemosensitive response as measured by HVR during induction to HA.

Acclimatization↗