Husain K

References (13)

Title : Phytochemical profile and diverse pharmacology of Garcinia celebica L - Mustafa_2024_Heliyon_10_e30629
Author(s) : Mustafa NH , Jalil J , Leong KE , Jamal JA , Husain K
Ref : Heliyon , 10 :e30629 , 2024
Abstract : Garcinia celebica L. syn. Garcinia hombroniana Pierre belongs to the family Clusiaceae, is indigenous to Southeast Asian countries. This review aims to provide updated, comprehensive and categorized information on the phytoconstituents and pharmacological effects of this species. The data collection mainly involved searches through databases named Scopus, Google Scholar, Pubmed and Springer Link. Approximately 100 phytochemicals were recorded in this review, with various classes of compounds such as triterpenoids, flavonoids, benzophenones, xanthones, depsidones and sterols identified. The most abundant compounds isolated belong to two chemical classes: triterpenoids and xanthones. Their extracts and pure compounds have been reported for their antibacterial, antiparasitic, hepatoprotective, antioxidant, antidiabetic, antituberculosis, antiplatelet aggregation, anti-neuraminidase and cholinesterase inhibitory activities. This review will provide a comprehensive understanding between the phytochemical components and its medicinal uses that may serve as a valuable resource for future drug development.
ESTHER : Mustafa_2024_Heliyon_10_e30629
PubMedSearch : Mustafa_2024_Heliyon_10_e30629
PubMedID: 38742069

Title : Pharmacological agents in the prophylaxis\/treatment of organophosphorous pesticide intoxication - Husain_2010_Indian.J.Exp.Biol_48_642
Author(s) : Husain K , Ansari RA , Ferder L
Ref : Indian J Exp Biol , 48 :642 , 2010
Abstract : Organophosphorus pesticide poisoning causes tens of thousands of deaths each year across the world. Poisoning includes acute cholinergic crisis as a result of AChE inhibition, intermediate syndrome (IMS) due to neuromuscular necrosis and organophosphate-induced delayed neuropathy (OPIDN) due to inhibition of neuropathy target esterase (NTE). Standard treatment for acute poisoning involves administration of intravenous atropine, oxime 2-PAM to counter AChE inhibition and diazepam for CNS protection. However clinical trials showed ineffectiveness of the standard therapy regimen. Although new oximes that can reactivate both peripheral and cerebral AChE and other prophylactic agents such as human serum butyrylcholinesterase (Hu BChE), sodium bicarbonate, huperzine A (a reversible ChE inhibitor) with imidazenil (a GABAA receptor modulator) have been proved effective in animal models, systematic clinical trials in patients are warranted. For IMS which is non-responsive to standard therapy, supportive therapy specifically artificial respiration followed by recovery is indicated. For OPIDN which has a different target (NTE) than AChE, standard therapy is ineffective. However neuroprotective drugs such as corticosteroids proved partially effective. Pretreatment with protease inhibitor PMSF has been shown to protect the aging of NTE and prevent the development of delayed symptoms in hens. Since the biology of NTE is being explored, new pharmacological agents should be developed in future. OP pesticide poisoning is a serious condition that needs rapid diagnosis and treatment. Since respiratory failure is the major reason for mortality, artificial respiration, careful monitoring, appropriate treatment and early recognition of OP pesticide poisoning may decrease the mortality rate among these patients.
ESTHER : Husain_2010_Indian.J.Exp.Biol_48_642
PubMedSearch : Husain_2010_Indian.J.Exp.Biol_48_642
PubMedID: 20929049

Title : Persistent\/delayed toxic effects of low-dose sarin and pyridostigmine under physical stress (exercise) in mice - Husain_2004_Indian.J.Physiol.Pharmacol_48_150
Author(s) : Husain K , Somani SM
Ref : Indian Journal de Physiologie Pharmacol , 48 :150 , 2004
Abstract : Pyridostigmine bromide, a reversible anticholinesterase drug, was used by military personnel during the Gulf War. They were under physical stress and might have been exposed to low-dose nerve gas, sarin. This study examined the interactions of low-dose sarin and pyridostigmine in exercised mice. Male NIH Swiss mice were treated as follows: 1) Control; 2) Sarin (0.01 mg/kg, sc); 3) exercise; 4) sarin plus exercise; 5) pyridostigmine; 6) pyridostigmine plus exercise; 7) pyridostigmine plus sarin; 8) pyridostigmine plus sarin plus exercise. Exercise was given daily for 10 weeks on treadmill and pyridostigmine and sarin were administered daily during the 5th and 6th weeks only. Respiratory exchange ratio decreased significantly during the dosing period of 5th and 6th weeks in groups 4, 6, and 8. Animals were sacrificed 24 hours after the ten-week exercise, tissues isolated and analyzed. Sarin significantly decreased butyrylcholine esterase (BChE) activity in plasma; AChE activity in platelet, triceps muscle, and striatum; neurotoxic esterase (NTE) activity in platelets, spinal cord, cortex and striatum and malondialdehyde (MDA) levels in sciatic nerve and cord. Sarin plus exercise significantly reduced BChE activity in plasma; acetylcholinesterase (AChE) activity in platelets, muscle, nerve and striatum; NTE activity in platelets, cord, cortex and striatum; and increased creatinine phosphokinase (CK) activity in plasma and MDA levels in cord. Pyridostigmine plus exercise significantly decrease BChE activity in plasma; AChE activity in muscle and enhanced malondialdehyde (MDA) levels in muscle. Pyridostigmine plus sarin significantly decreased NTE activity in platelets, cord, cortex and striatum. Pyridostigmine plus sarin plus exercise significantly altered AChE activity and MDA levels in muscle; and NTE activity in platelets, nerve, cord and cortex. Exercise significantly augmented the changes in plasma CK activity, muscle and nerve AChE activity, platelet NTE activity and cord MDA levels induced by sarin. It is concluded that physical stress (exercise) enhanced the persistent/delayed toxic effects of low-dose sarin and pyridostigmine in specific tissues of mice.
ESTHER : Husain_2004_Indian.J.Physiol.Pharmacol_48_150
PubMedSearch : Husain_2004_Indian.J.Physiol.Pharmacol_48_150
PubMedID: 15521554

Title : Interactive and delayed effects of pyridostigmine and physical stress on biochemical and histological changes in peripheral tissues of mice - Somani_2000_J.Appl.Toxicol_20_327
Author(s) : Somani SM , Husain K , Asha T , Helfert R
Ref : J Appl Toxicol , 20 :327 , 2000
Abstract : Gulf War veterans were taking pyridostigmine orally against possible exposure to nerve agents as well as being under physical stress. This study was designed to investigate the delayed effects of pyridostigmine and treadmill exercise on cholinesterase activity, lipid peroxidation and histology of peripheral tissues of mice. Male NIH Swiss mice were divided into four groups of 15 animals each and treated as follows: sedentary control; exercise training for 10 weeks; pyridostigmine (1.2 mg kg(-1), p.o.) for 2 weeks during weeks 5 and 6; and pyridostigmine plus exercise training. The mice were sacrificed 24 h after the last exercise, and blood, triceps muscle and sciatic nerve were isolated and analyzed. The group treated with pyridostigmine alone showed decreased plasma butyrylcholinesterase (BChE) activity (87% of control), whereas pyridostigmine plus exercise significantly decreased the BChE activity (79% of control), indicating an interactive effect of the combination. Acetylcholinesterase (AChE) activity did not alter significantly in red blood cells, platelets or sciatic nerve with either of the treatments. However, AChE activity in triceps muscle decreased significantly (78% of control) in the group treated with pyridostigmine plus exercise. Creatine phosphokinase activity in plasma increased slightly (compared to control, pyridostigmine or exercise group) in mice treated with pyridostigmine plus exercise, which may be indicative of perturbation in the integrity of the skeletal muscle due to combination. However, there were no obvious histological abnormalities in the triceps muscle detected between experimental and control groups. Interaction of pyridostigmine and exercise significantly increased the concentration of the end product of lipid peroxidation (malondialdehyde) (124% of control) in triceps muscle, indicating an oxidative stress response of the combination. These results indicate that physical stress enhanced the delayed toxic effects of a subchronic oral dose of pyridostigmine primarily in the skeletal muscle of mice.
ESTHER : Somani_2000_J.Appl.Toxicol_20_327
PubMedSearch : Somani_2000_J.Appl.Toxicol_20_327
PubMedID: 10942908

Title : Delayed effects of pyridostigmine and exercise training on acetylcholinesterase and muscle tension in mouse lower extremity - Verma-Ahuja_2000_Arch.Toxicol_74_539
Author(s) : Verma-Ahuja S , Husain K , Verhulst S , Espinosa JA , Somani SM
Ref : Archives of Toxicology , 74 :539 , 2000
Abstract : In this study, the interactive effects of pyridostigmine, a pretreatment drug against nerve agents, and exercise training on muscle tension were investigated in the mouse lower extremity anterior muscular compartment by dorsiflexion of the foot with stimulation of the peroneal nerve. Acetylcholinesterase (AChE), lipid peroxidation (in terms of the end-product malondialdehyde, MDA) and creatine phosphokinase (CPK) activity in the muscle were correlated with muscle tension. Male NIH Swiss mice were divided into four groups and treated as follows: (1) sedentary control; (2) pyridostigmine (1.2 mg/kg orally) daily for the 5th and 6th weeks; (3) exercise training for 10 weeks; and (4) pyridostigmine plus exercise training for 10 weeks. Experiments on muscle tension were conducted 4 weeks after the last dose of pyridostigmine or saline and 24 h after exercise. The muscle tension was measured in right and left legs using a tension transduction device connected to a polygraph. After muscle tension recording, mice were killed, blood and triceps muscle were isolated, and plasma CPK and muscle AChE activities, and MDA were determined. There was a significant increase in the muscle tension (P<0.05) in the group treated with pyridostigmine plus exercise as compared to the control and exercise groups. The pyridostigmine plus exercise group also showed a significant reduction in AChE activity (P<0.01) and enhanced MDA (P<0.05) in the triceps muscle. These results suggest that subchronic dosages of pyridostigmine and interaction with exercise training result in the delayed effects of reduction in muscle AChE activity and enhanced muscle tension.
ESTHER : Verma-Ahuja_2000_Arch.Toxicol_74_539
PubMedSearch : Verma-Ahuja_2000_Arch.Toxicol_74_539
PubMedID: 11131034

Title : Response of the olfactory bulb antioxidant system following diethyldithiocarbamate (DDTC) administration in rats - Struble_1999_J.Appl.Toxicol_19_221
Author(s) : Struble RG , Husain K , Somani SM
Ref : Journal of Applied Toxicology , 19 :221 , 1999
Abstract : This study was designed in order to evaluate alterations in the reactive oxygen species (ROS) scavenging system in olfactory bulb, dorsal neocortex and cerebellum for 6 weeks following a single subcutaneous dose (600 mg kg-1) of diethyldithiocarbamate (DDTC) to rats. A single dose of DDTC caused substantial damage to the olfactory epithelium and degeneration within the olfactory bulb. The epithelium regenerates, followed by regeneration in the olfactory bulb. The mean olfactory bulb weight decreased significantly 3 days after DDTC administration and gradually recovered to control values in 6 weeks. The DDTC-induced lesion of the olfactory nerve resulted in significant changes in glutathione (GSH) and antioxidant enzyme activities in olfactory bulb. In contrast, no significant changes were found in either cerebellum or dorsal neocortex. These observations indicate that a single dose of DDTC selectively affected the ROS scavenging system of the olfactory bulb. Moreover, these changes persisted for at least 6 weeks, which includes regeneration and synaptogenesis. Olfactory bulb GSH concentrations decreased significantly by 47 +/- 4%, glutathione reductase activity decreased by 18 +/- 3% and catalase activity increased by 27 +/- 7% over the 6 weeks. Superoxide dismutase activity decreased significantly in olfactory bulb of rats by 32 +/- 6% at 3 days following the lesion and then recovered and increased by 38 +/- 3% at 3 weeks. Olfactory bulb malondialdehyde concentrations were elevated (298 +/- 67%) throughout the post-lesion survival period, although this change did not reach the stringent statistical significance level required in this study. These data suggest that increased ROS flux perturbs the olfactory bulb antioxidant defense system during olfactory nerve regeneration.
ESTHER : Struble_1999_J.Appl.Toxicol_19_221
PubMedSearch : Struble_1999_J.Appl.Toxicol_19_221
PubMedID: 10439335

Title : Effect of exercise training and chronic ethanol ingestion on cholinesterase activity and lipid peroxidation in blood and brain regions of rat - Husain_1998_Prog.Neuropsychopharmacol.Biol.Psychiatry_22_411
Author(s) : Husain K , Somani SM
Ref : Prog Neuropsychopharmacol Biological Psychiatry , 22 :411 , 1998
Abstract : 1. This study examines the effects of exercise training and chronic ethanol consumption on cholinesterase activity and its relationship to lipid peroxidation in blood and brain regions of rat. 2. Exercise training (6.5 weeks) decreased acetylcholinesterase (AChE) activity significantly (64% of control) in hypothalamus and increased AChE activity in cerebral cortex (149% of control), whereas, malondialdehyde (MDA) levels increased in hypothalamus (129% of control) and decreased in cortex, striatum, and cerebellum (50%, 69% and 75% of control), respectively. 3. Chronic ethanol ingestion (2.0 gm/kg, p.o. for 6.5 weeks) significantly increased butyrylcholinesterase (BCHE) activity in plasma (136% of control) and decreased AChE activity in hypothalamus (63% of control), whereas, MDA levels increased in hypothalamus, cortex, and plasma (140%, 130% and 220% of control), respectively. 4. The combination significantly increased BCHE activity (173% of control) in plasma and decreased AChE activity (71% of control) in hypothalamus and (57% of control) in cerebellum, whereas, MDA levels increased in hypothalamus, cerebellum, medulla and plasma (134%, 128%, 140% and 309% of control), respectively. 5. Exercise training, chronic ethanol ingestion, and combination selectively inhibited hypothalamic AChE and the inhibition was correlated with increased lipid peroxidation (r = 0.11, 0.41 and 0.45) which may perturb hypothalamic function. The combination enhanced the peripheral stress response by increasing plasma BCHE activity and lipid peroxidation.
ESTHER : Husain_1998_Prog.Neuropsychopharmacol.Biol.Psychiatry_22_411
PubMedSearch : Husain_1998_Prog.Neuropsychopharmacol.Biol.Psychiatry_22_411
PubMedID: 98271537

Title : Influence of exercise and ethanol on cholinesterase activity and lipid peroxidation in blood and brain regions of rat - Husain_1997_Prog.Neuropsychopharmacol.Biol.Psychiatry_21_659
Author(s) : Husain K , Somani SM
Ref : Prog Neuropsychopharmacol Biological Psychiatry , 21 :659 , 1997
Abstract : 1. This study elucidates the interaction of acute exercise and single ethanol intake on cholinergic enzyme and its relationship to lipid peroxidation in the blood and brain regions of the rat. 2. Butyrylcholinesterase (BuChE) in plasma and acetylcholinesterase (AChE) in brain regions as well as lipid peroxidation (MDA) were assayed in 1) sedentary control rats; 2) after acute exercise (100% VO2max); 3) ethanol 20% (1.6 gm/kg, p.o.); 4) exercise and then ethanol 20% (1.6 gm/kg, p.o.). 3. Acute exercise significantly increased BuChE activity (155% of control) in plasma and decreased AChE activity (60% of control) in the corpus striatum with a significant increase in the striatal MDA level (254% of control). Ethanol significantly decreased AChE activity only in striatum (86% of control) with a significant increase in striatal MDA level (132% of control). 4. The combination of exercise and ethanol 20% (1.6 gm/kg, p.o.) significantly increased BuChE activity (123% of control) in plasma, and decreased AChE activity (76% of control) in striatum with significant increase in striatal MDA level (147% of control). 5. Acute exercise, single ethanol 20% (1.6 gm/kg, p.o.) intake and the combination selectively inhibited striatal AChE, and the inhibition was correlated with increased lipid peroxidation indicating perturbation of motor function. The combination reduced the peripheral stress response caused by exhaustive exercise.
ESTHER : Husain_1997_Prog.Neuropsychopharmacol.Biol.Psychiatry_21_659
PubMedSearch : Husain_1997_Prog.Neuropsychopharmacol.Biol.Psychiatry_21_659
PubMedID: 9194147

Title : Pharmacological Evaluation of Antidotes against Organophosphorus Intoxication -
Author(s) : Dube SN , Bhattacharya R , Husain K , Sikder AK
Ref : In Enzyme of the Cholinesterase Family - Proceedings of Fifth International Meeting on Cholinesterases , (Quinn, D.M., Balasubramanian, A.S., Doctor, B.P., Taylor, P., Eds) Plenum Publishing Corp. :375 , 1995
PubMedID:

Title : Protective Efficacy of Physostigmine and Pyridostigmine at Various Pretreatment Times against Inhaled Sarin in Rats -
Author(s) : Vijayaraghavan R , Husain K , Kumar P , Pandey KS , Das Gupta S
Ref : In Enzyme of the Cholinesterase Family - Proceedings of Fifth International Meeting on Cholinesterases , (Quinn, D.M., Balasubramanian, A.S., Doctor, B.P., Taylor, P., Eds) Plenum Publishing Corp. :408 , 1995
PubMedID:

Title : Phenyl valerate and choline ester hydrolases in the platelets of human, hen, rat and mouse - Husain_1994_Human.Exp.Toxicol_13_157
Author(s) : Husain K
Ref : Hum Exp Toxicol , 13 :157 , 1994
Abstract : 1. The levels of phenyl valerate and choline ester hydrolases in the platelets of human and certain laboratory animals have been determined for comparison. 2. The activities of total phenyl valerate hydrolase (PVase), paraoxon insensitive phenyl valerate hydrolase (PI-PVase), paraoxon and mipafox resistant esterase (PMRE) and propionyl-cholinesterase (PChE) were maximal in hen followed by mouse, rat and human. 3. Neurotoxic esterase (NTE) and acetylcholinesterase (AChE) activities were concentrated in the platelets of hens followed by humans, rats and mice in order. 4. Maximum concentration of butyrylcholinesterase (BChE) was found in the platelets of hens followed by mice, humans and rats. 5. It is concluded that the normal levels of enzyme activities in the platelets of humans and various species of animals may help to evaluate the exposure risk to neurotoxic organophosphorous compounds.
ESTHER : Husain_1994_Human.Exp.Toxicol_13_157
PubMedSearch : Husain_1994_Human.Exp.Toxicol_13_157
PubMedID: 7909676

Title : The 3,3'-bis-pyridinium mono-oximes as antidotes against organophosphorous intoxication - Sikder_1992_J.Pharm.Pharmacol_44_1038
Author(s) : Sikder AK , Pandey KS , Jaiswal DK , Dube SN , Kumar D , Husain K , Bhattacharya R , Das Gupta S
Ref : J Pharm Pharmacol , 44 :1038 , 1992
Abstract : In an attempt to develop effective antidotes against organophosphorous intoxication, three new structurally related bispyridinium mono-oximes with a 2-oxopropane bridge were synthesized. The compounds were evaluated for in-vivo therapeutic protection and cholinesterase reactivation in blood and various brain regions. In neuromuscular function studies against diisopropyl-fluorophosphate and isopropyl methylphosphonofluoridate poisoning, the oximes produced significant protection. The compounds produced marked peripheral reactivation and beneficial effects on neuromuscular transmission. The reactivation of cholinesterase in cerebral cortex by the oximes, in spite of their being quaternary salts is a notable feature.
ESTHER : Sikder_1992_J.Pharm.Pharmacol_44_1038
PubMedSearch : Sikder_1992_J.Pharm.Pharmacol_44_1038
PubMedID: 1361555

Title : Effectiveness of certain drugs in acute malathion intoxication in rats - Husain_1990_Ecotoxicol.Environ.Saf_19_271
Author(s) : Husain K , Ansari RA
Ref : Ecotoxicology & Environmental Safety , 19 :271 , 1990
Abstract : The protective effects of atropine, diacetylmonoxime (DAM), and diazepam separately and in combination were investigated in rats exposed to malathion. Malathion (500 mg/kg, ip) inhibited acetylcholinesterase (AchE) activity in RBC and brain and produced hyperglycemia and hyperlactacidemia with depletion of glycogen in liver, triceps, and brain of animals 2 hr after its administration. Atropine (20 mg/kg, ip) given immediately after malathion abolished hyperglycemia and glycogenolytic effect but exhibited no effect on the recovery of inhibited AchE activity. DAM (100 mg/kg ip) given immediately after malathion significantly reactivated the inhibited AchE activity both in RBC and brain. It also partially modified hyperglycemia and glycogenolytic effect. Diazepam (50 mg/kg, ip) slightly modified AchE and abolished hyperglycemia, hyperlactacidemia, and glycogenolytic effects. A combination of these drugs protected the animals from the acute toxic effects of malathion.
ESTHER : Husain_1990_Ecotoxicol.Environ.Saf_19_271
PubMedSearch : Husain_1990_Ecotoxicol.Environ.Saf_19_271
PubMedID: 2364909