The alleles that are detrimental to health, especially in older age, are thought to persist in populations because they also confer some benefits for individuals (through antagonistic pleiotropy). The ApoE4 allele at the ApoE locus, encoding apolipoprotein E (ApoE), significantly increases risk of poor health, and yet it is present in many populations at relatively high frequencies. Why has it not been replaced by natural selection with the health-beneficial ApoE3 allele? ApoE is a major supplier of cholesterol precursor for the production of ovarian oestrogen and progesterone, thus ApoE has been suggested as the potential candidate gene that may cause variation in reproductive performance. Our results support this hypothesis showing that in 117 regularly menstruating women those with genotypes with at least one ApoE4 allele had significantly higher levels of mean luteal progesterone (144.21 pmol l ⁻¹ ) than women with genotypes without ApoE4 (120.49 pmol l ⁻¹ ), which indicates higher potential fertility. The hormonal profiles were based on daily data for entire menstrual cycles. We suggest that the finding of higher progesterone in women with ApoE4 allele could provide first strong evidence for an evolutionary mechanism of maintaining the ancestral and health-worsening ApoE4 allele in human populations.

Air pollution can influence women’s reproductive health, specifically menstrual cycle characteristics, oocyte quality, and risk of miscarriage. The aim of the study was to assess whether air pollution can affect the length of the overall menstrual cycle and the length of its phases (follicular and luteal). Municipal ecological monitoring data was used to assess the air pollution exposure during the monitored menstrual cycle of each of 133 woman of reproductive age. Principal component analyses were used to group pollutants (PM₁₀, SO₂, CO, and NO_x) to represent a source-related mixture. PM₁₀ and SO₂ assessed separately negatively affected the length of the luteal phase after standardization (b = −0.02; p = 0.03; b = −0.06; p = 0.02, respectively). Representing a fossil fuel combustion emission, they were also associated with luteal phase shortening (b = −0.32; p = 0.02). These pollutants did not affect the follicular phase length and overall cycle length, neither in single- nor in multi-pollutant models. CO and NO_x assessed either separately or together as a traffic emission were not associated with overall cycle length or the length of cycle phases. Luteal phase shortening, a possible manifestation of luteal phase deficiency, can result from fossil fuel combustion. This suggests that air pollution may contribute to fertility problems in women.

The DNA damage in bone marrow cells induced by etoposide (E) injected intraperitoneally to rats (100 mg/kg b.w.) decreased to the control level when quercetin (Q) was administered subcutaneously for 10 consecutive days (40 mg/kg b.w.per day) before E was injected. The antioxidant power (FRAP assay) increased significantly after Q or E compared with control rats but did not change when Q preceded the E injection. The superoxide dismutase activity significantly increased in Q+E-treated rats compared with quercetin given alone. The study provides evidence that Q protects bone marrow cells against long-lived E-induced DNA damage and alters the redox balance in lung tissue.

Variation in the levels of sex-steroid hormones results from differences in developmental conditions, adult lifestyle, and genetic polymorphism. Genes involved in sex-steroid biosynthesis have been implicated to influence levels of hormones in premenopausal women, but the results were inconclusive. We tested variation among women in levels of salivary estradiol (E₂) corresponding to CYP17 genotypes. CYP17 encodes cytochrome P450c17α, which mediates two enzymes important in E₂ synthesis. In contrast to the earlier studies that relied on one or a few samples for assessing the E₂ levels of an individual woman, our study is based on daily collected saliva samples for one entire menstrual cycle. Sixty Polish women, ages 24 to 36 years, with regular menstrual cycles and no reported fertility problems participated in the study. Women with A2/A2 genotype had 54% higher mean E₂ levels than women with A1/A1 genotype (P = 0.0001) and 37% higher than women with A1/A2 genotype (P = 0.0008). Heterozygous A1/A2 women had 13 % higher E₂ levels than homozygous A1/A1 women (but this difference was significant only in a nonparametric test). Levels of E₂ during the day with highest E₂ (day −1) were 72% higher in A2/A2 compared with A1/A1 (P = 0.01) and 52 % higher compared with A1/A2 (P = 0.03). Our results suggest that CYP17 genotype may serve as a biomarker of endocrine function in women of reproductive age. (Cancer Epidemiol Biomarkers Prev 2006;15(11):2131–5)

The observed growth of cancer incidence in certain regions has been usually linked to frequent consumption of ‘unhealthy’ food. Such food often contains genotoxic substances as heterocyclic aromatic amines (HAAs) and/or polycyclic aromatic hydrocarbones (PAHs), occurring during food preparation, which induce DNA damage in cells. These substances are mainly formed during frying or grilling of meat and they can be removed from the body in a two-stage metabolic process of detoxification (phase 1 and phase 2). If they are not excreted, they form DNA adducts. The effectiveness of detoxification depends on the activity of enzymes encoded by polymorphic genes. A diet containing plenty of fruits and vegetables, due to the presence of biologically active polyphenols, can modulate activity of detoxifying enzymes. Such a diet can decrease the extent of DNA adducts, breaks and oxidative damage, supporting the body’s enzymatic system in sufficient removal of DNA damage. The antioxidant vitamins’ content in such a diet also enhances the DNA protection by increasing the scavenging of radical oxidative species that occurs during metabolic reactions. The lack of balance between the amount of ‘unhealthy’ and ‘healthy’ food leads to the accumulation of unrepaired damage, initiating DNA instability and inducing cancer development. Such damage is often used as a biomarker of cancer risk in epidemiological studies. Moreover, in in vitro studies, the amount of the DNA damage is used as indicator of the protective ability of vitamins, plant extracts and/or individual flavonoids. The incidences of certain dietaryrelated cancers in European Mediterranean countries is lower than in Central and Northern European countries; there is simultaneously variation in the habitual diet in these regions. This suggests that some features of routine nutrition in the Mediterranean countries may be responsible for this preventing effect. However, inconsistency in the epidemiological data, associating the meat and fruit and vegetable intake with cancer risk, suggests that another strategy for evaluation dietary influence on cancer risk should be undertaken. This article argues that it is not the consumption of a single food product or an individual component of diet, but rather a proper ratio of vegetable to meat consumption that is responsible for cancer prevention. This hypothesis is tested comparing the association between certain dietaryrelated cancer incidences (colon & rectum, breast and prostate cancer), registered in 2002, with the ratio between consumption of these two groups of food products in the Mediterranean region and in Central and Northern European region over the last three decades. The results clearly showed that both the ratio between vegetables and meat consumption as well as the ratio between the amount of energy from vegetables and from animal products can be used successfully to evaluate the dietary pattern related to cancer risk.