Previous human and experimental studies have demonstrated that lead exposure may modify the metabolism of lipids. Several studies have indicated that exposure to lead produces an increase in lipid peroxidation and inhibits blood superoxide dismutase activity. Recently, lipid peroxides have been shown to impair tissue membranes and to be a risk factor for vascular diseases. The aim of the present investigation was to evaluate the impact of subclinical lead poisoning on rat lipids in the context of atherosclerosis. The degree of poisoning was analogous to that in populations exposed to lead in a contaminated environment. Experiments were performed on male Buffalo rats with body weights of 150-200 g. The experimental animals received lead acetate intragastrically in doses of 35 mg lead/kg body wt. (Pb/kg) once weekly or 70 mg Pb/kg twice weekly for 7 weeks. Control rats were fed in the same manner with sodium acetate equimolar to the acetate in the lead acetate solution. One day after the feeding was over, venous blood samples, under ether anesthesia, were collected. The animals were killed by exsanguination and the liver was excised for determination of the metal (lead, copper, and zinc) content. A segment of the abdominal aorta was excised for histological examination. In venous blood the following were estimated: triglycerides, total cholesterol, high-density lipoprotein (HDL)-cholesterol fraction, serum lipid peroxides, and blood superoxide dismutase activity. Metal content (lead, copper, and zinc) in blood and liver was determined by means of atomic absorption spectrophotometry. In rats poisoned with small doses of lead, decreases in the plasma cholesterol level and the HDL-cholesterol fraction were observed.(ABSTRACT TRUNCATED AT 250 WORDS)

We report a case of a 27-year-old female with anemia, treated with high dose oral and parenteral iron therapy (within 20 days, the patient received a total dose of 4 g Fe+2 orally and 700 mg Fe+2 iv and im), and developed clinical manifestations characteristic of acute iron poisoning. Initial gastrointestinal symptoms and hypotension were followed by signs of mitochondrial toxicity: high leucocytosis, shock, multi-organ failure and disseminated intravascular coagulation. We discuss the difficulties in diagnosing acute iron poisoning. The initial low total iron blood capacity and high ferritin level, as well as the typical sequence of symptoms, supported the diagnosis. The patient avoided fatal consequences, probably due to the administration of iron doses over an extended period of time. However, cumulative effects led to the apparent iron toxicity. After 2 weeks of treatment, the patient was discharged from hospital in good condition. Human & Experimental Toxicology (2007) 26, 663-666

Cardiovascular diseases are still the main cause of death in Poland and throughout the world. Independent risk factors of cardiovascular disease, in addition to elevated LDL cholesterol, are both low HDL levels and high levels of non-HDL cholesterol. Plasma phospholipid-transfer protein (PLTP) and cholesteryl ester transfer protein (CETP) both play a major role in the metabolism of those lipoproteins. A lack of these proteins increases HDL and lowers LDL levels. In the light of current knowledge, it seems reasonable to search for compounds that may decrease the activity of CETP, and thus reduce the incidence of cardiovascular disease. Whereas on the one hand there are reports about the adverse effect of torcetrapib and the lack of therapeutic effects of dalcetrapib, on the other hand the question arises whether the CETP inhibitors that are currently in clinical trials will rise to the challenges before them. Currently, it is known that the activity of PLTP, while affecting the metabolism of lipoproteins, especially HDL, plays a major role in atherogenesis. Still, there are some contradictions and controversies about the effect of PLTP on reverse cholesterol transport (RCT). There are a number of studies about the role that PLTP plays in the pathogenesis of various diseases. Further studies are needed to clearly determine the impact of PLTP activity on the formation and development of pathological processes in the cardiovascular system.

A b s t r a c tBackground: Linseed oil has cardio-protective effects. However, its antihypertensive action has not yet been well characterised. Aim:The primary purpose of the study was to evaluate the effect of short-term dietary supplementation with linseed oil on blood pressure (BP) and lipid metabolism in patients with mild hypercholesterolaemia. The secondary aim was to assess the effect of linseed oil on nitric oxide pathway and selected serum trace metals.Methods: 150 volunteers: 43 men (49.9 ± 11.5 years) and 107 women (53.2 ± 10.3 years), diagnosed with mild hypercholesterolaemia, were assessed prospectively for BP and lipid levels, before and after lipid-lowering diet plus linseed oil supplementation at a dose of 15 mL daily for four weeks (study groups) or four-weekly lipid-lowering diet (control group). Multivariate logistic regression analysis was used to determine the effect of linseed oil on BP after adjustment for age, sex, height, body weight, body mass index, smoking status, and alcohol consumption.Results: Supplementation with linseed oil significantly decreased low-density lipoprotein (LDL)-and non-high-density lipoprotein (HDL) cholesterol, and increased HDL-and HDL 3 -cholesterol levels. Additionally, linseed oil decreased diastolic BP in men (95% confidence interval [CI]: -6.0 to -1.1, p < 0.006), whereas in women linseed oil reduced (p < 0.001) systolic BP (-3.6 mmHg; 95% CI: -5.8 to -1.5) as well as diastolic BP (-4 mmHg; 95% CI: -5.8 to -2.1). Women with higher BP displayed an increase in serum L-arginine level (p < 0.01). In the logistic regression model oil consumption was associated with a decrease in mean BP (adjusted odds ratio 3.85; 95% CI 1.32-11.33). Conclusions:Our findings confirm the benefit of short-term linseed oil use in mild hypercholesterolaemia, particularly in patients with increased blood pressure.