Risk factors for atherosclerosis in students of a private university in São Paulo-Brazil.

OBJECTIVE: To characterize the risk profile for atherosclerosis (AS) in adolescents and young adults of a private university in São Paulo. METHODS: Clinical, nutritional, and laboratory parameters were evaluated in 209 students of both genders aged 17 to 25 years. In addition to determination of the lipid profile, the association of its abnormal values with other risk factors for AS was also investigated. RESULTS: Increased levels of total cholesterol, LDL-C and triglycerides (TG) were observed in 9.1%, 7.6% and 16.3% of the students, respectively, and decreased levels of HDL-C in 8.6% of them. Prevalence of the remaining risk factors analyzed was elevated: sedentary life style (78.9%); high intake of total fat (77.5%); high cholesterol intake (35.9%); smoking, hypertension (15.8%) and obesity (7.2%). There was an association between elevated LDL-C and TG levels and sedentary life style and body mass index. CONCLUSION: The high prevalence of risk factors for AS in young individuals draws attention to the need for adopting preventive plans.

Cocaine mutagenicity and hepatocarcinogenicity evaluations in rodents.

The mutagenicity (clastogenicity) and the carcinogenicity (promoting potential) of cocaine were evaluated, respectively, by the mouse bone marrow micronucleus test (study I) and by the initiated rat liver bioassay (study II). In study I, two administration routes (i.p. and i.v.) and two sampling times (24 and 48 hours) after cocaine treatment were studied. Swiss male mice were treated with cocaine at doses of 0, 18, 37, and 75 mg/kg and 0, 2, 4, and 8 mg/kg by i.p. and i.v. routes, respectively. No significant differences were observed between treated and negative control groups regarding the frequencies of micronuclei and the polichromatic/normochromatic erythrocyte (PCE/NCE) ratios. In study II, the development of putative preneoplastic foci of hepatocytes expressing the enzyme glutathione S-transferase placental form (GST-P+) was utilized as the end-point marker in a 8-week rat liver bioassay. The animals were initiated for carcinogenesis by a single i.p. sub-carcinogenic dose of diethylnitrosamine (DEN). After a 6-week exposure to 5 or 10 mg/kg of cocaine i.v. twice a week there was no enhancement of GST-P+ foci development above the values of the control DEN-only treated animals. Also, cocaine did not induce any toxicity as evidenced by the absence of alterations of rat body and liver weights and of liver biochemical function and morphology. The results suggest that cocaine does not have a mutagenic effect on the mouse bone marrow cells or promoting activity on the rat hepatocarcinogenesis process.