The relationship of problem gambling to criminal behavior in a sample of Canadian male federal offenders.

This article examines the prevalence of moderate and severe problem gambling in a sample of 254 incarcerated Canadian male federal offenders (completion rate of 39.0%). The prevalence of disordered gambling was measured using the PGSI, DSM-IV-TR, and SOGS that yielded estimates of 9.4%, 6.3%, and 13.0%, respectively. Severe problem gamblers were significantly more likely to have committed income producing offences, but were neither more nor less likely than other offenders to have committed violent offences. The majority of severe problem gamblers (65.2%) and a fifth of the moderate problem gamblers (20.0%) reported that their criminal activity was a result of their gambling (e.g., to pay off debts). Based on these findings there appears to be a need to offer problem gambling treatment services to offenders in order to help them break the cycle of gambling, debt and crime.

Modulation of neurotoxic behavior in F-344 rats by temporal disposition of benzo(a)pyrene.

The behavioral changes caused by benzo(a)pyrene (BaP), a polycyclic aromatic hydrocarbon (PAH) compound, were monitored, and also its metabolite levels in cerebellum and cortex were measured in BaP treated rats to see if any relationship existed between these two aspects. Rats were administered 0, 25, 50, 100, and 200 mg/kg of BaP in peanut oil by oral gavage. Plasma, and brain tissue (cerebellum and cortex) samples were collected at 0, 2, 4, 6, 12, 24, 48, 72 and 96 h post administration. Neurotoxic effects peaked at 2 h after dosing and lasted 48 h after dosing for all dose groups. The metabolite levels remained the same from 2 to 4 h, reached a peak at 6 h post gavage and showed a gradual decline returning to baseline levels at 72 h when the motor activity of treatment groups also returned to control levels, indicating recovery from the effects of BaP. A significant (P<0.05) correlation between neurotoxic effects and BaP plasma, and brain metabolite concentrations suggests that metabolism plays an important role in modulating the neurobehavioral effects of BaP.

Benzo(a)pyrene-induced acute neurotoxicity in the F-344 rat: role of oxidative stress.

Given the link between neurotoxicity and exposure to pollutants, the potential behavioral neurotoxicity of benzo(a)pyrene [B(a)P] was investigated. Studies have established that B(a)P requires metabolic activation to highly reactive species to elicit many of its adverse effects. This study investigated the perturbation of nervous system function by correlating behavioral changes with the metabolism of B(a)P, antioxidant enzyme levels and lipid peroxidation in selected brain regions. The neurobehavioral effects of single oral doses of B(a)P (25-200 mg kg(-1) body weight) on motor activity were examined in male F-344 rats at 2, 4, 6, 12, 24, 48, 72 and 96 h post treatment. Parent B(a)P and metabolites were measured at the above mentioned time points by reverse phase HPLC. The activity of several antioxidant enzymes (superoxide dismutase, catalase and glutathione peroxidase) and levels of malondialdehyde were determined at 6 and 96 h in both the striatum and hippocampus of B(a)P exposed rats. Suppression of motor activity (up to 70%) reached a maximum at 6 h, but was reversible at 96 h in all dose groups. The kinetics of disposition data show a strong link between B(a)P metabolism and the onset and duration of behavioral effects. Benzo(a)pyrene caused a 15-70% inhibition in the activity of superoxide dismutase and glutathione peroxidase and an enhancement in catalase and lipid peroxidation (up to 68%) in the striatum and hippocampus at 6 and 96 h post treatment, respectively. These findings suggest that B(a)P-induced acute neurobehavioral toxicity may occur through oxidative stress due to inhibition of the brain antioxidant scavenging system.

Fluoranthene-induced neurobehavioral toxicity in F-344 rats.

Fluroanthene (FLA) is a nonalternant representative of polycyclic aromatic hydrocarbon (PAH) family of toxic chemicals that are widely distributed in the environment. The effects of single acute doses of FLA on locomotor activities and the functional observational battery (FOB) were investigated in 8-week-old male and female F-344 rats. FLA was dissolved in peanut oil and administered by oral gavage as single doses of 0, 100, 200 and 400 mg/kg. Immediately after dosing, animals were placed in activity cages and monitored for nocturnal locomotor activities at 2-hour intervals and for a total of 12 hours for 5 consecutive days post treatment. Significant (p <.001) reductions in horizontal activity, total distance, stereotypy, and vertical activity were observed. Rats administered acute doses of FLA were also subjected to the functional observational battery (FOB) tests that were conducted at 0, 2, 4, 6, 12, 24, 48, 72 and 96 hours after FLA administration. FLA-exposed animals showed significant (p <.05) dysfunction, including ataxia, decreased grip strengths, increased landing foot splay, loss of aerial righting, increased urination and defecation, and decreased responses to sensory stimuli in both sexes. Neurological deficits in the FOB peaked at 6 hours and lasted for 48 hours post treatment. Significant (p <.05) gender-related differences were noted in behavioral end points, with male rats showing greater sensitivity to FLA administration than females, as evidenced by their greater mean severity scores in FOB parameters and lower motor activity counts. These findings suggest that FLA can produce behavioral toxicity in F-344 rats and that motor activity and the FOB may serve as end points for the detection of acute FLA toxicity.