Raushan Husain

BEHAVIORAL, NEUROCHEMICAL, AND NEUROMORPHOLOGICAL EFFECTS OF DELTAMETHRIN IN ADULT RATS

The neurotoxic action of a synthetic pyrethroid, a deltamethrin formulation (Decis), was studied in adult rats. Adult male albino rats received deltamethrin in formulation at a dose of 7.0 mg/kg body weight/d in corn oil orally for 15 d. Deltamethrin-exposed rats exhibited a decrease in body weight from d 9 onward, which was significantly lowered at d 15 of exposure. Administration of deltamethrin markedly increased the wet weight of the hippocampus and pons medulla region without much affecting the weight of frontal cortex, corpus striatum, hypothalamus, and cerebellum. A significant increase in the activity of monoamine oxidase was observed in frontal cortex, hippocampus, and cerebellum, and acetylcholinesterase activity was markedly increased in frontal cortex, corpus striatum, hippocampus, cerebellum, and pons medulla. The activity of Na+,K(+)-ATPase showed marked decrease in frontal cortex, hippocampus, and cerebellum following deltamethrin exposure. The polyamine concentration in brain regions was significantly affected, and all three polyamines showed marked alterations in the cerebellum. Deltamethrin significantly increased the spontaneous locomotor activity and aggressive behavior. Maze learning was markedly decreased. Morphological changes in Purkinje neurons in the cerebellum were observed in deltamethrin-exposed rats. Results suggest significant neurochemical and neuromorphological changes, which may culminate in perturbed synaptic function following deltamethrin exposure in rats.

Effect of styrene on levels of serotonin, noradrenaline, dopamine and activity of acetyl cholinesterase and monoamine oxidase in rat brain

Oral intubation of styrene (1 ml/kg body weight daily) in adult male albino rats for 15 days produced a significant increase in serotonin and noradrenaline but no change in dopamine contents in brain. The brain of treated animals also showed a significant decrease in monoamine oxidase (MAO) but no change in acetyl cholinesterase (AChE) activity. The neurotoxic effects of styrene may be mediated through alterations in levels of these biogenic amines in the brain tissue.

Chelation in metal intoxication: I. In vivo effect of chelating agents on liver and testis of manganese administered rats

Abstract Ability of some structurally different chelating agents to mobilize manganese from liver and testis of rats pretreated with manganese sulphate for 25 days, was evaluated. Attempts were made to draw a parallel between removal of the metal and recovery of the altered biochemical and pathological parameters in early manganese poisoning. Though all the compounds were able to remove manganese significantly from the two organs, a definite relationship was exhibited by nitrilotriacetic acid, diethylenetriaminepentaacetic acid and p -aminosalicylic acid.

Intrahippocampal cholinergic-rich transplants restore lead-induced deficits: a preliminary study in rats.

In the present study restorative potential of fetal cholinergic rich cell suspensions in ameliorating cognitive deficits in rats perinatally exposed to lead was studied. Lactating dams with 1-day old litters were given 0.2% (w/v) lead acetate in drinking water throughout lactation from postnatal day (PND) 1 to PND21 at the end of which the treatment was stopped and the animals were weaned. On PND42 lead exposed rats were given bilateral, intrahippocampal, cholinergic rich fetal neural transplants (approximately 60,000 cells per site) and subsequently assessed 3 and 6 months posttransplantation. Control animals (Sham operated and transplanted) were also run in parallel. Lead exposed rats exhibited a decreased learning ability and locomotor activity. A significant decrease in the levels of acetylcholinesterase and sodium potassium ATPase Na+,K+-ATPase activity was observed in hippocampal region of lead exposed rats. The levels of lead were increased by fivefold in the hippocampal region of lead exposed rats. Transplantation showed marginal improvement in the above impairments at 3 months which were more marked at 6 months. Lead levels at 6 months were not significantly higher in lead exposed rats as compared with the control. Results confirm previous findings that fetal neural transplants help in restoring the lost functional deficits and demonstrate their restorative potential in case of lead induced deficits.

Influence of Iron Deficiency and Lead Treatment on Behavior and Cerebellar and Hippocampal Polyamine Levels in Neonatal Rats

Effect of lead exposure and iron-deficiency on polyamine levels in neuronal and glial cells of cerebellum and hippocampus was investigated in weaned rats. Lactating dams with one day old litters were given 0.2% (w/v) lead acetate in drinking water from postnatal day one to twenty one and maintained on an iron-deficient diet. There was an overall reduction of putrescine, spermidine and spermine in neuronal and glial cells of cerebellum and hippocampus consequent to lead exposure and iron-deficiency alone. Lead exposure and iron-deficiency together did not potentiate the polyamine levels in neuronal and glial cells of cerebellum and hippocampus uniformly. However, the enhanced lowering of putrescine in the hippocampal glia, spermidine in cerebellar neuronal and spermine in both neuronal and glial cells of cerebellum during the critical stage of brain development may result in stunted neuronal growth and sprouting in lead exposed and iron-deficient animals. The behavioral alterations as observed in the present study may be due to impaired neuronal development resulting from a depressed polyamine pathway and which could be attributed to cognitive deficits in growing children.

Acrylamide induced inhibition of hepatic glutathione-S-transferase activity in rats.

Rats injected i.p. with acrylamide (50 mg/kg/day) for 5 days showed a significant inhibition of hepatic glutathione-S-transferase (GST) activity; maximum inhibition occurred in 15-day-old rats in which early development of hind limb paralysis was noted. Addition of acrylamide in vitro to the assay system also inhibited GST activity. No changes were observed in oxidized and reduced glutathione contents.

Increased neurobehavioral toxicity of styrene in protein-malnourished rats

Influence of protein deficiency on the neurobehavioral toxicity of styrene during gestation and early infancy was studied in rats. Eye opening and fur growth were delayed in rat pups born to dams receiving a low protein diet. These pups also showed a delay in the development of surface and air righting reflexes and cliff avoidance response and a marginal increase in the levels of dopamine and serotonin receptors in comparison to those born to dams receiving a normal protein diet. Alterations in these parameters were more marked in pups born to dams exposed to styrene and receiving a low protein diet. In addition, these pups also showed a significant decrease in the activity of monoamine oxidase, Na+, K(+)-ATPase and succinic dehydrogenase as well as significant increases in motor activity and receptor sensitivity when compared to rat pups born to dams receiving a low protein diet. No significant alterations in behavioral and biochemical parameters were observed in the pups born to dams exposed to styrene and receiving a normal protein diet at this dose level. These results suggest that protein deficiency during early life renders the animals more susceptible to styrene.

Influence of di-butyltin dilaurate on brain neurotransmitter systems and behavior in rats

Exposure to DBTL (20, 40 or 80 mg/kg body weight) caused a decrease in levels of noradrenaline (NA), dopamine (DA) and serotonin (5-HT) at all treatment levels. Hypothalamus and frontal cortex appeared to be most affected, since levels of all the three amines examined showed changes in these areas. Maximum decrease of DA was found in corpus striatum, NA in pons medulla and of 5-HT in frontal cortex. These animals also showed a decrease in spontaneous locomotor activity and learning at all the doses. The data indicates involvement of hypothalamus and frontal cortical regions of the brain in the neurotoxicity of DBTL.

Methyl methacrylate induced behavioural and neurochemical changes in rats.

Methyl methacrylate (MMA), a widely used monomer in the manufacture of acrylic polymers, has been reported to cause neurological deficits in industrial workers. The effect of MMA on regional brain biogenic amines and their correlation with behavioural responses were examined. Male Wistar rats received orally MMA (500 mg/kg body wt) for 21 consecutive days. Our results indicate that MMA markedly impaired locomotor activity and learning, while aggressive behaviour significantly increased. An overall enhancement of biogenic amine levels in pons-medulla and hippocampus was noted. In addition, for noradrenaline an increase in cerebral cortex and corpus striatum, for 5-hydroxytryptamine an increase in mid-brain and hypothalamus and for dopamine a slight decrease in corpus striatum were recorded. The changes in regional brain biogenic amine levels may be partly responsible for altered behaviour.

Some behavioral effects of early styrene intoxication in experimental animals

Male albino rats were administered styrene in groundnut oil, PO at doses of 100 mg and 200 mg/kg body weight daily for 14 consecutive days. No neurological deficit was observed in any animal during the course of the experiment. Mean % avoidance response (learning) for each treated group, from day 1 to day 4 of conditioned avoidance response training, revealed a general increase. Styrene significantly increased the % avoidance response at both doses as compared to controls, although no definite dose-response relationship was evident. No significant difference was noted in the spontaneous locomotor activity and regional brain catecholamine levels, between controls and treated rats of either dose. Serotonin levels in hippocampus, hypothalamus, and mid-brain were significantly raised at the higher dose of styrene. Therefore, elevated serotonin levels in these brain regions may account for styrene-induced learning.