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F Islam

Publications and source records attributed to F Islam.

At least 19 recordsLinked to original sources

Zingiber officinale exhibits behavioral radioprotection against radiation-induced CTA in a gender-specific manner.

At the organismic level, exposure to radiation can produce taste aversion (CTA) learning and emesis, which have been proposed as behavioral endpoints that are mediated by harmful effects of radiations on peripheral systems, primarily the gastrointestinal system. Thus, the aim of the present investigation was to study the gastroprotective action of hydroalcoholic extract of zingiber rhizome (Zingiber officinale Rosc.) against radiation-induced conditioned taste aversion (CTA) in both male and female species of animals, for testing its potential as a behavioral radioprotector. Administration of zingiber extract 1 h before 2-Gy gamma-radiation was significantly effective in blocking the saccharin avoidance response, with 200 and 250 mg/kg b.wt. i.p., being the most effective doses for male and female rats, respectively. A comparison of the efficacy of zingiber extract with two antiemetic drugs, ondansteron and dexamethasone, revealed that the extract rendered comparable protection against radiation-induced CTA. Our experiments also confirmed the existence of sex dichotomy (i.e., the sex of animal greatly influenced response towards radiation exposure) in relation to behavioral responses (CTA) or differential metabolism. The observed gender variations were hypothesized to be a result of hormonal fluctuations and differences in pharmacological parameters in male and female rats. To correlate the mechanism of action, the free-radical-scavenging potential of zingiber extract to scavenge hydroxyl ion and nitric oxide was also tested, in cell-free system and a concentration of 1000 microg/ml, was found to be the most potent, which has been proposed as one the many activities assisting in its overall ability to modulate radiation-induced taste aversion. The results demonstrate that Z. officinale possesses antioxidant, radioprotective and neuromodulatory properties that can be effectively utilized for behavioral radioprotection and for efficiently mitigating radiation-induced CTA in both males and females species.

Animals↗

Zingiber officinale Rosc. modulates gamma radiation-induced conditioned taste aversion.

The aim of the present study was to investigate the neurobehavioral protective efficacy of a hydroalcoholic extract of ginger (Zingiber officinale Rosc.) in mitigating gamma radiation-induced conditioned taste aversion in Sprague-Dawley rats. Administration of Zingiber extract 1 h before 2-Gy gamma irradiation was effective in blocking the saccharin avoidance response for 5 post-treatment observational days, both in a dose- and time-dependent manner, with 200 mg/kg b.w. i.p. being the most effective dose. Highest saccharin intake in all the groups was observed on the fifth post-treatment day. The potential of ginger extract to inhibit lipid peroxidation induced by radiation (2 Gy) and ascorbate-ion stress in brain homogenate and its ability to scavenge highly reactive superoxide anions were evaluated. The 1000-microg/ml and 2000-microg/ml concentration of ginger extract showed the highest efficiency in scavenging free radicals and in inhibiting lipid peroxidation. The lipid peroxidation and superoxide-anion scavenging ability of the extract further supports its radioprotective properties. The results clearly establish the neurobehavioral efficacy of ginger extract and the antioxidant properties appear to be a contributing factor in its overall ability to modulate radiation-induced conditioned taste aversion. Ginger extract has tremendous potential for clinical applications in mitigation of radiation-induced emesis in humans.

Animals↗

Arsenic concentrations in rice, vegetables, and fish in Bangladesh: a preliminary study.

Arsenic contaminating groundwater in Bangladesh is one of the largest environmental health hazards in the world. Because of the potential risk to human health through consumption of agricultural produce grown in fields irrigated with arsenic contaminated water, we have determined the level of contamination in 100 samples of crop, vegetables and fresh water fish collected from three different regions in Bangladesh. Arsenic concentrations were determined by hydride generation atomic absorption spectrophotometry. All 11 samples of water and 18 samples of soil exceeded the expected limits of arsenic. No samples of rice grain (Oryza sativa L.) had arsenic concentrations more than the recommended limit of 1.0 mg/kg. However, rice plants, especially the roots had a significantly higher concentration of arsenic (2.4 mg/kg) compared to stem (0.73 mg/kg) and rice grains (0.14 mg/kg). Arsenic contents of vegetables varied; those exceeding the food safety limits included Kachu sak (Colocasia antiquorum) (0.09-3.99 mg/kg, n=9), potatoes (Solanum tuberisum) (0.07-1.36 mg/kg, n=5), and Kalmi sak (Ipomoea reptoms) (0.1-1.53 mg/kg, n=6). Lata fish (Ophicephalus punctatus) did not contain unacceptable levels of arsenic. These results indicate that arsenic contaminates some food items in Bangladesh. Further studies with larger samples are needed to demonstrate the extent of arsenic contamination of food in Bangladesh.

Agriculture↗

Mosquito repellent (pyrethroid-based) induced dysfunction of blood-brain barrier permeability in developing brain.

Pyrethroid-based mosquito repellents (MR) are commonly used to protect humans against mosquito vector. New born babies and children are often exposed to pyrethroids for long periods by the use of liquid vaporizers. Occupational and experimental studies indicate that pyrethroids can cause clinical, biochemical and neurological changes, and that exposure to pyrethroids during organogenesis and early developmental period is especially harmful. The neurotoxicity caused by MR has aroused concern among public regarding their use. In the present study, the effect of exposure of rat pups during early developmental stages to a pyrethroid-based MR (allethrin, 3.6% w/v, 8h per day through inhalation) on blood-brain barrier (BBB) permeability was investigated. Sodium fluororescein (SF) and Evan's blue (EB) were used as micromolecular and macromolecular tracers, respectively. Exposure during prenatal (gestation days 1-20), postnatal (PND1-30) and perinatal (gestation days 1-20 + PND1-30) periods showed significant increase in the brain uptake index (BUI) of SF by 54% (P < 0.01), 70% (P < 0.01), 79% (P < 0.01), respectively. This increase persisted (68%, P < 0.01) even 1 week after withdrawal of exposure (as assessed on PND37). EB did not exhibit significant change in BBB permeability in any of the group. The results suggest that MR inhalation during early prenatal/postnatal/perinatal life may have adverse effects on infants leading to central nervous system (CNS) abnormalities, if a mechanism operates in humans similar to that in rat pups.

Aging↗

Presence of alpha-1 adrenoreceptors on thermosensitive neurons in the medial preoptico-anterior hypothalamic area in rats.

Earlier microinjection studies showed that norepinephrine in the medial preoptico-anterior hypothalamic area (mPOAH) regulates body temperature and the action is mediated through alpha-1 adrenoceptors. This study was conducted to confirm if the thermosensitive neurons in the mPOAH of rats possess alpha-1 adrenoceptors. First, the thermosensitivity of mPOAH neurons was tested and then the effects of microiontophoretic application of prazosin, alpha 1 adrenoceptor antagonist, on the firing rate of both the thermosensitive as well as the insensitive neurons were recorded. Prazosin significantly inhibited the firing rate of the thermosensitive neurons suggesting that most of the cold and warm sensitive neurons in the mPOAH possess alpha-1 adrenoceptors. These results at the single neuronal level confirm our earlier hypothesis that in the mPOAH, norepinephrine regulates body temperature by acting on alpha-1 adrenoceptors. The data also suggest that sensitivity of the mPOAH neurons to norepinephrine alter with changes in body temperature. The detailed physiological significance of the results with special reference to thermoregulation at the single neuronal level has been discussed.

Adrenergic alpha-Antagonists↗

Steroidogenic alterations in testes and sera of rats exposed to formulated Fenvalerate by inhalation.

Fenvalerate (Fen) is a synthetic pyrethroid, which is commonly used for destroying a variety of insect pests damaging several vegetable, fruit, and cotton crops. This insecticide is also used to mitigate household insects like flies, cockroaches, mosquitoes, and so forth. Human beings are exposed to formulated Fen preparations mostly by inhalation during spraying in fields for crop protection, for control of household insects, and also during handling and packaging at manufacturing plants. Limited online information is available regarding toxic effects of formulated Fen exposure on mammalian reproductive system. The present study has been undertaken to investigate male reproductive toxic effects of a formulated preparation of Fen (20% EC) particularly in relation to steroidogenic alterations in testes and sera of rats exposed by nose-only inhalation for (4 hours/day and five days a week) for three months. The results indicate significant reduction in the weight of testes, epididymal sperm counts, and sperm motility, along with decrease in marker testicular enzymes for testosterone biosynthesis viz. 17-beta-hydroxy steroid dehydrogenase (17-beta-HSD) and glucose-6-phosphate dehydrogenase (G6PDH), leading to net decrease in serum testosterone concentration in group of rats exposed to one-fifth LC50 of Fen (20% EC) by inhalation (4 hours/day, five days a week) subchronically for three months. These results for the first time indicate the role of testosterone in Fen (20% EC)-induced male reproductive toxicity of rats subchronically exposed by inhalation probably due to neuroendocrine-mediated phenomenon and hormone-disrupting property of the insecticide.

17-Hydroxysteroid Dehydrogenases↗

GABA exerts opposite influence on warm and cold sensitive neurons in medial preoptic area in rats.

The preoptic area regulates body temperature. GABA-ergic terminals and receptors are present in this area. Local microinjection studies have shown that GABA, its agonist, and its antagonist in this area may modulate body temperature. However, there are warm and cold sensitive neurons, and they are known to be affected by local and peripheral temperatures. In order to understand the mechanism of action of GABA in temperature regulation at the cellular level it was necessary to study the effect of GABA on individual thermosensitive neurons in in vivo preparations. Hence, in this study the responses of preoptic area thermosensitive and insensitive neurons to microiontophoretic application of picrotoxin, a GABA-A antagonist, were studied in anaesthetized rats. It was observed that a majority of both the thermosensitive and insensitive neurons were affected by microiontophoretic application of picrotoxin. Although almost an equal number of cold and warm sensitive neurons were affected, a majority of the cold sensitive neurons were excited, while a majority of the warm sensitive neurons were inhibited by picrotoxin. The results suggested that in normal conditions GABA acts through GABA-A receptor in modulating the spontaneous activity of thermosensitive neurons in the preoptic area. Furthermore, the results of the present study taken together with other reports suggest that normally GABA exerts a direct inhibitory action on the cold sensitive neurons, while it acts on presynaptic heteroreceptors, possibly on norepinephrinergic afferent input terminals on the warm sensitive neurons, for mediating its action.

Animals↗

Methamphetamine-induced alteration in striatal p53 and bcl-2 expressions in mice.

Methamphetamine (METH)-induced alterations in the expression of p53 and bcl-2 protein were studied in the striatum of wild type, neuronal nitric oxide synthase knockout (nNOS -/-) and copper zinc superoxide dismutase overexpressed (SOD-Tg) mice. METH treatment up-regulated p53 and down-regulated bcl-2 expression in the striatum of wild type mice. No significant alterations were observed in the expression of these proteins in the nNOS -/- or SOD-Tg mice. These data suggest that METH might cause its neurotoxic effects via the production of free radicals and secondary perturbations in the expression of genes known to be involved in apoptosis and cell death machinery.

Animals↗

Role of wake inducing brain stem area on rapid eye movement sleep regulation in freely moving cats.

Some of the characteristic symptoms associated with rapid eye movement (REM) sleep are opposite to, while some apparently resemble, those of wakefulness. Therefore, it was hypothesised that the neurons present in the wakefulness inducing area(s) in the brain are likely to communicate with the REM sleep related neurons. Brain stem neurons were classified based on their firing rates in relation to electrophysiological correlates associated with spontaneous sleep and wakefulness recorded from freely moving, normally behaving cats. Thereafter, the responses of those classified neurons to stimulation of brain stem reticular wakefulness inducing area were studied. Results from 63 neurons showed that the wake inducing area affected 62% of the neurons. Fifty-eight percent of the neurons which increased firing during wakefulness, including the REM-OFF neurons, were excited, while 70% of the neurons which decreased firing during wakefulness, including the REM-ON neurons, were inhibited. These observations support our hypothesis and, along with their physiological significance, are discussed.

Action Potentials↗

Peroxynitrite plays a role in methamphetamine-induced dopaminergic neurotoxicity: evidence from mice lacking neuronal nitric oxide synthase gene or overexpressing copper-zinc superoxide dismutase.

The use of methamphetamine (METH) leads to neurotoxic effects in mammals. These neurotoxic effects appear to be related to the production of free radicals. To assess the role of peroxynitrite in METH-induced dopaminergic, we investigated the production of 3-nitrotyrosine (3-NT) in the mouse striatum. The levels of 3-NT increased in the striatum of wild-type mice treated with multiple doses of METH (4 x 10 mg/kg, 2 h interval) as compared with the controls. However, no significant production of 3-NT was observed either in the striata of neuronal nitric oxide synthase knockout mice (nNOS -/-) or copper-zinc superoxide dismutase overexpressed transgenic mice (SOD-Tg) treated with similar doses of METH. The dopaminergic damage induced by METH treatment was also attenuated in nNOS-/- or SOD-Tg mice. These data further confirm that METH causes its neurotoxic effects via the production of peroxynitrite.

Animals↗

Pulmonary toxicity of a formulated preparation of fenvalerate in rats subchronically exposed by nose only inhalation for 90 days.

OBJECTIVE: The pulmonary toxicity of a commercially available formulated preparation of Fenvalerate (Fen), a synthetic pyrethroid has been studied in rats following subchronic nose only inhalation exposure route. METHOD: Adult male rats were exposed to Fen for 4 h/day, 5 days a week for 90 days by using Flow Past Dynamic Nose only Inhalation Chamber. RESULTS: Fen exposed rats showed a significant increase in enzymatic activities of lactate dehydrogenase (LDH), acid phosphatase (ACP), alkaline phosphatase (ALP) and gamma-glutamyl transferase (gamma-GT) which are considered as biochemical indicators of pulmonary damage. The concomitant histopathological examination of Fen exposed rats' lung revealed inflammatory changes viz., influx of mononuclear cells admixed with a few giant cells in alveolar lumen, hypetrophied bronchiolar and alveolar epithelial lining cells and presence of edematous fluid in alveolar lumen alongwith congested parenchymatous blood vessels. CONCLUSION: These results for the first time indicate the pulmonary toxic effects of a commonly used formulated Fen preparation by using rat model and nose only inhalation as the route of exposure.

Animals↗

Prevention of dopaminergic neurotoxicity by targeting nitric oxide and peroxynitrite: implications for the prevention of methamphetamine-induced neurotoxic damage.

Methamphetamine (METH) is a neurotoxic psychostimulant that produces catecholaminergic brain damage by producing oxidative stress and free radical generation. The role of oxygen and nitrogen radicals is well documented as a cause of METH-induced neurotoxic damage. In this study, we have obtained evidence that METH-induced neurotoxicity is the resultant of interaction between oxygen and nitrogen radicals, and it is mediated by the production of peroxynitrite. We have also assessed the effects of inhibitors of neuronal nitric oxide synthase (nNOS) as well as scavenger of nitric oxide and a peroxynitrite decomposition catalyst. Significant protective effects were observed with the inhibitor of nNOS, 7-nitroindazole (7-NI), as well as by the selective peroxynitrite scavenger or decomposition catalyst, 5,10,15,20-tetrakis(2,4,6-trimethyl-3,5-sulfonatophenyl)porphyrinato iron III (FeTPPS). However, the use of a nitric oxide scavenger, 2-phenyl-4,4,5,5-tetramethylimidazoline-1-oxyl-3-oxide (c-PTIO), did not provide any significant protection against METH-induced hyperthermia or peroxynitrite generation and the resulting dopaminergic neurotoxicity. In particular, treatment with FeTPPS completely prevented METH-induced hyperthermia, peroxynitrite production, and METH-induced dopaminergic depletion. Together, these data demonstrate that METH-induced dopaminergic neurotoxicity is mediated by the generation of peroxynitrite, which can be selectively protected by nNOS inhibitors or peroxynitrite scavenger or decomposition catalysts.

3,4-Dihydroxyphenylacetic Acid↗

Selenium altered the levels of lipids, lipid peroxidation, and sulfhydryl groups in straitum and thalamus of rat.

The effect of sodium selenite (0.05, 0.1, and 0.2 mg/kg body weight, i.p.) on the lipid levels (total lipids, phospholipids, cholesterol, gangliosides), thiobarbituric acid reactive substance (TBARS), and sulfhydryl group (-SH) in the striatum and thalamus of a male Wistar rat was studied after 7 d of treatment. The level of total lipids and cholesterol was significantly and dose-dependently elevated in the striatum and thalamus with 0.1 and 0.2 mg/kg of sodium selenite. However, the cholesterol level was significantly increased only with 0.2 mg/kg of sodium selenite in the thalamus. The level of phospholipids and gangliosides was more significant with 0.1 mg/kg of sodium selenite as compared to 0.2 mg. No significant alteration on the gangliosides level was observed in the thalamus with various doses of sodium selenite although the elevation with 0.2 mg dose was 25.9%. The content of TBARS was elevated dose dependently in striatum, but its level was depleted significantly with 0.1-mg/kg dose of sodium selenite in the thalamus. The level of the -SH group was significantly depleted in the striatum with 0.1-mg/kg dose of sodium selenite; conversely, this dose has significantly elevated the levels of -SH group in the thalamus.

Animals↗

Methamphetamine generates peroxynitrite and produces dopaminergic neurotoxicity in mice: protective effects of peroxynitrite decomposition catalyst.

Methamphetamine (METH)-induced dopaminergic neurotoxicity is believed to be produced by oxidative stress and free radical generation. The present study was undertaken to investigate if METH generates peroxynitrite and produces dopaminergic neurotoxicity. We also investigated if this generation of peroxynitrite can be blocked by a selective peroxynitrite decomposition catalyst, 5, 10,15, 20-tetrakis(N-methyl-4'-pyridyl)porphyrinato iron III (FeTMPyP) and protect against METH-induced dopaminergic neurotoxicity. Administration of METH resulted in the significant formation of 3-nitrotyrosine (3-NT), an in vivo marker of peroxynitrite generation, in the striatum and also caused a significant increase in the body temperature. METH injection also caused a significant decrease in the concentration of dopamine (DA), 3, 4-dihydroxyphenylacetic acid (DOPAC), and homovanillic acid (HVA) by 76%, 53% and 40%, respectively, in the striatum compared with the control group. Treatment with FeTMPyP blocked the formation of 3-NT by 66% when compared with the METH group. FeTMPyP treatment also provided significant protection against the METH-induced hyperthermia and depletion of DA, DOPAC and HVA. Administration of FeTMPyP alone neither resulted in 3-NT formation nor had any significant effect on DA or its metabolite concentrations. These findings indicate that peroxynitrite plays a role in METH-induced dopaminergic neurotoxicity and also suggests that peroxynitrite decomposition catalysts may be beneficial for the management of psychostimulant abuse.

3,4-Dihydroxyphenylacetic Acid↗