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Biomedical subjects

J J Ghosh

Publications and source records attributed to J J Ghosh.

At least 19 recordsLinked to original sources
PubMed1996

Protective role of anion channel blocker in lipid peroxidation caused by H2O2 in microsomes of bovine pulmonary arterial smooth muscle tissue.

The role of hydroxyl radical (OH.) in H2O2-mediated stimulation of lipid peroxidation in microsomes of bovine pulmonary arterial smooth muscle tissue and the protective effects of DIDS, the anion channel blocker have been studied. Treatment of microsomes with H2O2 (1 mM) stimulate iron release, OH. production and lipid peroxidation. Pretreatment with DFO (an iron chelator) or DMTU (a hydroxyl radical scavenger) prevents OH. production and thereby reduces lipid peroxidation without any appreciable reduction of iron release. Simultaneous treatment of either DFO or DMTU with H2O2 significantly reduces lipid peroxidation and prevents OH. production without any significant reduction of iron release. However, addition of DFO or DMTU 2 min after treatment of the microsome with H2O2 does not produce any significant reduction of lipid peroxidation, OH production and iron release. Pretreatment of microsomes with DIDS markedly reduces the stimulation of lipid peroxidation without appreciably altering the increase in OH. production and iron release caused by H2O2.

4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid↗
PubMed1996

Redox state of pyridine nucleotides, but not glutathione, regulate Ca2+ release by H2O2 from mitochondria of pulmonary smooth muscle.

Treatment of bovine pulmonary artery smooth muscle mitochondria with H2O2 stimulated oxidation of GSH and NAD(P)H along with an increase in Ca2+ release. Addition of oxaloacetate to mitochondrial suspension stimulated Ca2+ release and oxidation of NAD(P)H while GSH level remained unchanged. Subsequently, addition of beta-hydroxybutyrate which reduced mitochondrial pyridine nucleotides caused reuptake of the released Ca2+ without causing appreciable alteration of GSH level. Treatment of the mitochondria with 1,3-bis(2-dichloroethyl)-1-nitrosourea (BCNU), an inhibitor of glutathione reductase, significantly decreased GSH level without producing discernible change in Ca2+ release and NAD(P)H oxidation.

Animals↗
PubMed1990

Inflammatory responses induced by substance P in rat paw.

Substance P (SP) injection in the plantar region of rat hind paw caused a dose related inflammation, which reached a peak within 10 min of injection and declined after 60 min. Low doses (0.25-0.063 mg/kg) of SP-antagonists like (D-Pro2, D-Trp7,9)-SP and (D-Pro2, D-Phe7, D-Trp9)-SP pretreatment significantly inhibited the SP induced paw oedema, while higher doses (0.5-1 mg/kg) showed agonistic effects. Pretreatment with diphenhydramine alone or along with low doses of SP-antagonists was highly significant in blocking this inflammation, the latter combination being more effective than the former. Pretreatment with acute capsaicin produced a synergestic effect on SP induced paw oedema, while pretreatment with chronic capsaicin significantly inhibited this SP induced paw oedema. The results indicate involvement of histamine and possible therapeutic importance of capsaicin in SP mediated inflammatory type of responses.

Animals↗
PubMed1985

Comparative toxic effect of sumithion on rat and pigeon at the level of myelin.

Both rats and pigeons treated with sumithion, an organophosphorous pesticide, at a daily oral dose of one-tenth of the LD50, die after the 6th exposure. In spinal cord myelin of pigeon cerebroside, sulphatide and total protein contents decrease by 30, 15.7 and 40.8%, respectively, and cholesterol increases by 30% after 5 days of treatment; that of the rat shows none of these changes. Densitometric scannings of sodium dodecylsulphate-polyacrylamide gels of myelin proteins show a decrease in Wolfgram and proteolipid protein in rats and in pigeons up to 3 days; after 5 days this change continues only in pigeons, whereas rats show a normal pattern. The proteolipid protein and basic protein of both the species show increased mobility towards the anode up to 3 days, whereas after 5 days this trend continues in pigeons but not in rats.

Animals↗
PubMed1985

A study of the distribution pattern of lead in the leaves of banyan trees (Ficus benghalensis) from different traffic density regions of Calcutta.

The accumulation of lead from motor vehicle exhaust on leaves of banyan trees (Ficus benghalensis) growing on roadsides from different traffic density regions of Calcutta has been investigated and the values have been compared with a few samples from remote areas. The analysis has been performed during the summer (April-July) and winter (November-January) months to study the effect of seasonal variations, if any. The results indicate that in high and medium traffic regions, lead content of banyan leaves is high and is more prominent in winter months than in summer months. Such changes due to seasonal variations are not marked in low and zero traffic density regions. This preliminary investigation demonstrates a general indication of the distribution pattern of lead in plants exposed to motor vehicle exhaust along a relatively busy thoroughfare of the city of Calcutta.

India↗
PubMed1985

Delta-9-Tetrahydrocannabinol: effect on mitochondrial swelling of different tissues of rat.

In vivo delta-9-tetrahydrocannabinol (delta-9-THC) under short (10 and 50 mg/kg) and long term (10 mg/kg/day for 15 consecutive days) administration (i.p.) to adult male albino rats increased the mitochondrial swelling of hypothalamus, heart and liver. Similarly, in vitro treatment with delta-9-THC (2-8 micrograms/mg protein) produced a dose-dependent stimulation in the mitochondrial swelling of different tissues. Ca2+ ions (0.15 mM - 0.3 mM) increased the mitochondrial swelling. Calcium (0.3 mM)-induced stimulation of mitochondrial swelling was enhanced with delta-9-THC under both in vivo and in vitro conditions. Chaotropic agents e.g. KNO3 (100-200 mM) and KSCN (200-400 mM), decreased the mitochondrial swelling. Chaotropic (200 mM)-induced inhibitory effect in different tissues was reduced with delta-9-THC under in vivo and in vitro treatments. These results suggest that delta-9-THC, like calcium, stimulated the mitochondrial swelling, and that the action of delta-9-THC may be localized on the specific structures of the membrane which are sensitive to chaotropic agents.

Animals↗
PubMed1984

Sumithion induced neurotoxicity in pigeons: effect on lipid metabolism of spinal cord.

Sumithion, a well known organophosphorus pesticide, produces hind leg paralysis and ataxia in pigeons at a dose of 5 mg/kg for 5 days. Histochemical changes in the spinal cord showed demyelination in the anterior portion of the thoracic region. Decreases in cholesterol, cerebroside and sulphatide and increases in cholesterol ester suggest demyelination in pigeons as a consequence of the neurotoxic effect of sumithion.

Animals↗
PubMed1984

Morphine inhibition of the insulin-inducible form of hepatic tyrosine aminotransferase.

Morphine treatment in normal intact rats caused a dose-dependent increase in hepatic tyrosine aminotransferase (TAT) activity, as demonstrable up to 2 hr of exposure to the opioid alkaloid. However, such increase in TAT activity was invariably preceded by a prior decline in the enzyme level, as observed after 15 min of morphine treatment. Such an initial decline in activity was not demonstrable in diabetic animals. Further studies indicate that morphine inhibited the insulin-induced increase in TAT activity, a phenomenon which could be reversed by the opioid antagonist naloxone. The results suggest an opioid control mechanism in the regulation of the insulin-inducible form of TAT and indicate the possibilities of a trophic role of endogenous opiates in gluconeogenesis.

Animals↗
PubMed1984

Role of adrenal steroids on electroacupuncture analgesia and on antagonising potency of naloxone.

Electroacupuncture (EA), a form of transcutaneous electrical stimulation, produces opiate-like antinociception and catalepsy in rats. This effect of EA cannot be produced in hypophysectomised rats, whereas adrenalectomised rats show increased sensitivity. In intact rats, adrenocorticotrophic hormone and dexamethasone have been found to be effective to sensitise the animals to the analgesic effect of EA. Deoxycorticosterone, on the contrary, attenuates this effect. Spironolactone is also effective to potentiate EA response, which is accompanied with severe respiratory depression. Drugs that are known to affect adrenal aldosterone secretion also modulate the effect of EA. Naloxone administration, 15 min prior to the initiation of EA stimulation, potentiates the effect of EA, whereas it counteracts the effect of EA if administered after initiation of EA stimulation. Moreover, this counteracting ability of naloxone increases with the increase in time interval between initiation of stimulation and naloxone challenge. Pretreatment with drugs that impair adrenal mineralocorticoid response to physiological stimuli inhibits the counteracting effect of naloxone. On the contrary, mineralocorticoid supplemented rats show greater sensitivity to naloxone counteraction.

Adrenal Glands↗
PubMed1983

Ovarian steroids and modulation of morphine-induced analgesia and catalepsy in female rats.

The influence of ovarian steroids on modulation of antinociceptive and cataleptic responses to morphine in female rats was evaluated. The sensitivity of the animals to morphine varied at different stages of the estrous cycle. The responses of postpartum and ovariectomized rats to morphine was attenuated. The test doses of estradiol-17 beta or progesterone, either alone or in combination, did not alter this attenuated morphine sensitivity. Testosterone, however, sensitized post-partum as well as ovariectomized rats to morphine. Unlike progesterone, 17-alpha-hydroxy progesterone antagonized testosterone. Collectively these data implicate ovarian testosterone as a physiological modulator of actions of morphine in female rats.

Analgesia↗
PubMed1983

Effects of chloroquine on lysosomal enzymes, NADPH-induced lipid peroxidation, and antioxidant enzymes of rat retina.

Chloroquine (1, 5 and 10 mg/kg), given in acute and in chronic (7 and 15 days) treatment schedules, caused characteristic alterations in the lysosomal enzyme system, antioxidant enzymes, NADPH-induced lipid peroxidation, and glutathione content in the retina of the rat. One-half hour and four hours after chloroquine administration, increased free activities of lysosomal enzymes and NADPH-induced lipid peroxidation were observed, associated with a decrease in tissue glutathione content. In contrast to the acute effect, chloroquine, given in 7- and 15-day treatment schedules, had no significant effect on the lysosomal enzyme system, while at the same time a normalization or a decrease in NADPH-induced lipid peroxidation, associated with a significant increase in tissue glutathione content, was noted. Catalase and peroxidase activities were decreased after both the acute and the daily treatment schedules. Superoxide dismutase activity, although increased in the high dose acute study, appeared otherwise little affected by chloroquine treatment.

Acetylglucosaminidase↗
PubMed1983

Modification of morphine antinociceptive response by blood glucose status: possible involvement of cellular energetics.

The antinociceptive response to morphine was enhanced in insulin-hypoglycemic animals whereas it was decreased in diabetic or in hypertonic glucose-pretreated hyperglycemic animals. 3-O-Methylglucose was, however, without effect on morphine analgesia whereas 2-deoxyglucose sensitized this effect. Furthermore, as malate and isocitrate attenuated the morphine analgesic response of insulin hypoglycemic animals and 2,4-dinitrophenol sensitized this response in diabetic animals, it is possible that the blood glucose level affects the morphine analgesic response by affecting cellular energetics.

Analgesia↗
PubMed1983

Electroacupuncture and its effect on rat hepatic functions.

The effect of single, acute (7 pulses/sec., 0.75 volt) and chronic (4 pulses/sec., 0.75 volt) electroacupuncture (EA) treatment on alternate days for a period of 21 days on hepatic functions of rats were studied at cellular and subcellular levels. The points used for EA were Shenshu, Dachangshu and Zusanli. After chronic treatment, (a) protein, RNA, phospholipid, and cholesterol contents of whole liver and liver microsomal fraction increased significantly, (b) liver microsomal G-6-Pase activity increased significantly, (c) microsomal lipid peroxidation value decreased, (d) lipase activity increased. After acute treatment, (e) phospholipid, and cholesterol contents of the whole liver and liver microsomal fraction increased significantly, (f) liver microsomal G-6-Pase activity increased significantly, (g) liver microsomal lipid peroxidation value decreased, (h) GPT and lipase activity of liver increased. The parameters unchanged in acute treatment were as follows: (i) protein, RNA content, (j) GOT activity of the liver, (k) SGOT and SGPT activity, (1) hepatic triglyceride. The parameters unchanged in chronic treatment were as follows: (m) GOT and GPT activity of the liver, (n) SGOT and SGPT activity, (o) hepatic triglyceride. No apparent harmful effect of EA on rat hepatic functions is obvious from present study.

Acupuncture Therapy↗
PubMed1982

Adrenal involvement in captopril-induced potentiation of morphine analgesia.

The involvement of the angiotensin-adrenal system as a possible mechanism in the potentiation of morphine analgesia by the angiotensin-converting enzyme inhibitor, captopril (SQ 14225), was studied in rats. Captopril pretreatment sensitized the animals to the analgesic effects of morphine while angiotensin II exerted an attenuating influence. These effects, however, were not demonstrable in adrenalectomized animals. Although captopril could inhibit the plasma angiotensin-converting enzyme activity, it appeared to have no significant effect on the brain enzyme. It has been suggested that the effects of captopril and angiotensin II on morphine analgesia are mediated indirectly through their effects on adrenal function.

Adrenal Glands↗
PubMed1982

Possible physiological role of adrenal and gonadal steroids in morphine analgesia.

The effects of adrenal and gonadal steroids on the antinociceptive potency of parenteral morphine were studied in male rats. At all doses studied, dexamethasone pretreatment 30 min before morphine sensitized the animals to the effects of parenteral morphine. However, at higher doses of dexamethasone this sensitization was masked when dexamethasone was given 4 h before morphine by a cycloheximide-sensitive attenuating effect. This feature is not a specific glucocorticoid effect since testosterone showed similar characteristics. Estradiol-17beta and progesterone, however, produced only a cycloheximide-sensitive attenuating response at 4 h. Deoxycorticosterone on the contrary had a cycloheximide-independent attenuating influence with both pretreatment schedules. Results of the present study indicate that morphine subsensitivity after castration or supersensitivity after adrenalectomy may be attributed to the relative lack of testosterone or mineralocorticoid in the respective conditions. Furthermore, in view of the fact that testosterone plays a rate-limiting role in determining the morphine sensitivity of the animals and that mineralocorticoids exert their effects indirectly via antagonism of testosterone action.

Adrenalectomy↗