Anticancer Activity of Encapsulated Pearl Millet Polyphenol-Rich Extract against Proliferating and Non-Proliferating Breast Cancer Cells In Vitro.

Plant-derived polyphenols are bioactive compounds with potential health-promoting properties including antioxidant, anti-inflammatory, and anticancer activity. However, their beneficial effects and biomedical applications may be limited due to their low bioavailability. In the present study, we have considered a microencapsulation-based drug delivery system to investigate the anticancer effects of polyphenol-rich (apigenin, caffeic acid, and luteolin) fractions, extracted from a cereal crop pearl millet (Pennisetum glaucum), using three phenotypically different cellular models of breast cancer in vitro, namely triple negative HCC1806, ER-positive HCC1428, and HER2-positive AU565 cells. Encapsulated polyphenolic extract induced apoptotic cell death in breast cancer cells with different receptor status, whereas it was ineffective against non-tumorigenic MCF10F cells. Encapsulated polyphenolic extract was also found to be cytotoxic against drug-resistant doxorubicin-induced senescent breast cancer cells that were accompanied by increased levels of apoptotic and necrotic markers, cell cycle inhibitor p21 and proinflammatory cytokine IL8. Furthermore, diverse responses to the stimulation with encapsulated polyphenolic extract in senescent breast cancer cells were observed, as in the encapsulated polyphenolic extract-treated non-proliferating AU565 cells, the autophagic pathway, here cytotoxic autophagy, was also induced, as judged by elevated levels of beclin-1 and LC3b. We show for the first time the anti-breast cancer activity of encapsulated polyphenolic extract of pearl millet and postulate that microencapsulation may be a useful approach for potentiating the anticancer effects of phytochemicals with limited bioavailability.

Neuroprotective effects of magnesium against stress induced by hydrogen peroxide in Wistar rat.

INTRODUCTION: Oxidative stress has been implicated in the pathogenesis of diverse disease states. The present study was designed to examine the effects of magnesium sulphate (MgSO4) against hydrogen peroxide (H2O2) induced behaviour impairment and oxidative damage in rats. MATERIAL AND METHODS: Eighteen rats were equally divided into three groups. The first group was kept as a control. In the second group, H2O2 was given in drinking water at 3% during 5 days. In the third group, rats were subjected to daily administration of H2O2 and MgSO4 (100 mg/kg; b.w) for 5 days. Animals were subjected to behavioural tests (elevated plus maze and open field). At the end of experiment, brains were extracted for oxidative stress biomarkers assessment including levels of malondialdéhyde and hydrogen peroxide and activities of superoxide dismutase and catalase. RESULTS: Our findings showed that H2O2 treated rat exhibited anxiogenic behaviour and the genesis of free radicals in the brain. Magnesium showed amelioration against oxidative stress and significant decrease in anxiety levels. DISCUSSION AND CONCLUSION: Stress is a powerful process that disrupts brain homeostasis by inducing oxidative stress and its appear that magnesium may have potential therapeutic benefits by reducing oxidative stress and inducing anxiolytic effect.

Exposure to 2.45 GHz Radiation Triggers Changes in HSP-70, Glucocorticoid Receptors and GFAP Biomarkers in Rat Brain.

Brain tissue may be especially sensitive to electromagnetic phenomena provoking signs of neural stress in cerebral activity. Fifty-four adult female Sprague-Dawley rats underwent ELISA and immunohistochemistry testing of four relevant anatomical areas of the cerebrum to measure biomarkers indicating induction of heat shock protein 70 (HSP-70), glucocorticoid receptors (GCR) or glial fibrillary acidic protein (GFAP) after single or repeated exposure to 2.45 GHz radiation in the experimental set-up. Neither radiation regime caused tissue heating, so thermal effects can be ruled out. A progressive decrease in GCR and HSP-70 was observed after acute or repeated irradiation in the somatosensory cortex, hypothalamus and hippocampus. In the limbic cortex; however, values for both biomarkers were significantly higher after repeated exposure to irradiation when compared to control animals. GFAP values in brain tissue after irradiation were not significantly different or were even lower than those of nonirradiated animals in all brain regions studied. Our results suggest that repeated exposure to 2.45 GHz elicited GCR/HSP-70 dysregulation in the brain, triggering a state of stress that could decrease tissue anti-inflammatory action without favoring glial proliferation and make the nervous system more vulnerable.

The Effects of Carob (Ceratonia siliqua L.) on Emotional Behavior Impairment and Metabolic Disorders Induced by Estrogen Deficiency in Rats.

Carob (Ceratonia siliqua L.) contains a wide variety of polyphenols with high antioxidant properties. In this study, we investigated the effects of aqueous extract of carob pods (AECP) on emotional behavior impairments and metabolic disorders in ovariectomized (OVX) rats. Female Wistar rats were assigned to three groups: group 1, control non-OVX rats; group 2, OVX rats; and group 3, OVX rats orally treated with AECP (500 mg/kg) for15 days after ovariectomy. Elevated plus-maze and open-field tests were performed on the 26th and 27th post-ovariectomy days, respectively. Afterwards, the rats were anesthetized and their serums were collected for biochemical analysis. We found that AECP improved emotional behavior impairments revealed by elevated plus-maze and open-field tests in OVX rats. Moreover, ovariectomy significantly increased triglyceride, lactate dehydrogenase, alanine aminotransferase, and aspartate aminotransferase levels in the serum. AECP administration significantly reversed ovariectomy-induced biochemical alterations. Thus, we suggest that the AECP may have an anxiolytic-like effect and prevent biochemical disorders associated with menopause or ovariectomy.

Zinc improves clomipramine effects on depressive and locomotor behavior and reverses its oxidative stress in rats.

Depression is a common mental disease affecting a lot of people of all ages around the world. Today, improving the therapeutic effects of currently used antidepressants such as clomipramine and, especially when they are administered at high doses is a topic of interest. The study aims to evaluate the eventual role of zinc (30 mg/Kg) in ameliorating clomipramine (75 mg/Kg) effects on behavior and oxidative stress equilibrium following a 6 day treatment in male Wistar rats. Our main findings showed that zinc improved clomipramine antidepressant and locomotor effects. Moreover, zinc reversed the oxidative stress induced by this drug in the liver. Thus, zinc at 30 mg/Kg may constitute an efficient adjuvant for clomipramine used at a high dose (75 mg/Kg) by boosting its efficacy on behavior and alleviating its negative effects on oxidative balance in liver.

Effect of sub-chronic ferrous sulfate treatment on motor skills, hematological and biochemical parameters in rats.

This study investigated the effects of ferrous sulfate (FeSO4) on motor skills, hematological and biochemical parameters in rats. Adult rats were treated with dose of iron (280 mg/L, per os) for 15 consecutive days in drinking water. No significant difference was noticed for the motor skills in the stationary beam (p = 0.23) and suspended string tests (p = 0.48) between control and iron-treated rats. However, iron-treated rats showed a significant increase in white blood cells count (p = 0.01), mean corpuscular volume values (p = 0.02) and decrease in frequency of peristaltic contractions of the fragment of the intestine (in vitro) compared to control rats (p = 0.01). No significant difference in plasma iron level (p = 0.89) and transferrin amount were observed after iron treatment (p = 0.65). The findings indicate that iron treatment at 280 mg/L, per os for 15 consecutive days in adult rats induced increase of hematological parameters (sign of a potential inflammation), but not motor skills deficit.

Effects of Smoking Exposure in Infants on Gastroesophageal Reflux as a Function of the Sleep-Wakefulness State.

OBJECTIVE: To determine whether perinatal smoking exposure is associated with gastroesophageal reflux (GER)-related changes in sleep-wakefulness states in neonates. STUDY DESIGN: Thirty-one neonates, referred for the investigation of suspected GER, were recruited and underwent multichannel impedance-pH monitoring and synchronized 8- to 12-hour polysomnography. The infants' exposure to tobacco smoke was estimated by means of a urine cotinine assay. The total number, frequency (h-1), and mean duration (minutes) of GER-pH (reflux events detected by the pH electrode only) and GER-imp (reflux events with bolus movement detected by impedance) events were determined. Intergroup differences (smoking-exposed group vs nonexposed group) were probed with nonparametric, unpaired Mann-Whitney U tests. A χ2 test was used to assess a possible intergroup difference in bolus retrograde migration during GER-imp events. RESULTS: According to the urine cotinine assay, 21 of the 31 neonates had been exposed to cigarette smoke during the perinatal period. The number (and frequency) of GER-imp was significantly greater (P = .016) in the exposed group (29 [0-90]) than in the nonexposed group (12 [2-35]). Migration of the esophageal bolus from the distal segment to the most proximal segment was significantly more frequent (P = .016) in the exposed group (83% of GER) than in the nonexposed group (41%). The GER pattern associated with smoking exposure was particularly obvious during Rapid eye movement sleep. CONCLUSIONS: The more frequent occurrence and greater proximal migration of GER-imp in the smoking-exposed group (especially during rapid eye movement sleep) may have clinical relevance. Smoking exposure is a preventable risk factor for limiting the occurrence of GER in neonates.

Pistacia lentiscus oil attenuates memory dysfunction and decreases levels of biomarkers of oxidative stress induced by lipopolysaccharide in rats.

Pistacia lentiscus L. is a well-known medicinal plant that has been used for its antioxidant, anti-inflammatory, neuroprotective, and hepatoprotective effects. However, the neuroprotective effect of Pistacia lentiscus oil (PLo) of has not been reported. The present study was designed to examine the neuroprotective and hepatoprotective effects of PLo aigainst lipopolysaccharide (LPS)-induced memory impairment and oxidative damage in rats. Twenty-four adult male Wistar rats were equally divided into three groups. The first group was kept as a control. In the second group, LPS was given at the single dose of 1 mg/kg intraperitoneally (i.p.). In the third group, PLo (3.3 mL/kg; per orally (p.o.)) was administered daily for 15 days, and challenged with LPS (1 mg/kg; i.p. injection two h before behavioral test). Thereafter, memory was assessed using spatial object recognition test. Cholinesterase activity and oxidative stress response were estimated in brain tissues and liver. PLo attenuated LPS-induced memory impairment in spatial object recognition test (p < 0.05). LPS treatment caused significant oxidative damage via induction of lipid peroxidation and reductions antioxidant defense system potency in the brain tissue and liver. Moreover, LPS increased brain activity of acetylcholinesterase and butyrylcholinesterase activity in the liver. The present results suggest that the beneficial effects of PLo on memory impairment of LPS-treated rats may be due to its protective effects against oxidative stress damage presumably via its antioxidant property.

Postnatal development and behavior effects of in-utero exposure of rats to radiofrequency waves emitted from conventional WiFi devices.

The present work investigated the effects of prenatal exposure to radiofrequency waves of conventional WiFi devices on postnatal development and behavior of rat offspring. Ten Wistar albino pregnant rats were randomly assigned to two groups (n=5). The experimental group was exposed to a 2.45GHz WiFi signal for 2h a day throughout gestation period. Control females were subjected to the same conditions as treated group without applying WiFi radiations. After delivery, the offspring was tested for physical and neurodevelopment during its 17 postnatal days (PND), then for anxiety (PND 28) and motricity (PND 40-43), as well as for cerebral oxidative stress response and cholinesterase activity in brain and serum (PND 28 and 43). Our main results showed that the in-utero WiFi exposure impaired offspring neurodevelopment during the first seventeen postnatal days without altering emotional and motor behavior at adult age. Besides, prenatal WiFi exposure induced cerebral oxidative stress imbalance (increase in malondialdehyde level (MDA) and hydrogen peroxide (H2O2) levels and decrease in catalase (CAT) and superoxide dismutase (SOD) activities) at 28 but not 43days old, also the exposure affected acethylcolinesterase activity at both cerebral and seric levels. Thus, the current study revealed that maternal exposure to WiFi radiofrequencies led to various adverse neurological effects in the offspring by affecting neurodevelopment, cerebral stress equilibrium and cholinesterase activity.

Effects of repeated restraint stress and WiFi signal exposure on behavior and oxidative stress in rats.

Today, due to technology development and aversive events of daily life, Human exposure to both radiofrequency and stress is unavoidable. This study investigated the co-exposure to repeated restraint stress and WiFi signal on cognitive function and oxidative stress in brain of male rats. Animals were divided into four groups: Control, WiFi-exposed, restrained and both WiFi-exposed and restrained groups. Each of WiFi exposure and restraint stress occurred 2 h (h)/day during 20 days. Subsequently, various tests were carried out for each group, such as anxiety in elevated plus maze, spatial learning abilities in the water maze, cerebral oxidative stress response and cholinesterase activity in brain and serum. Results showed that WiFi exposure and restraint stress, alone and especially if combined, induced an anxiety-like behavior without impairing spatial learning and memory abilities in rats. At cerebral level, we found an oxidative stress response triggered by WiFi and restraint, per se and especially when combined as well as WiFi-induced increase in acetylcholinesterase activity. Our results reveal that there is an impact of WiFi signal and restraint stress on the brain and cognitive processes especially in elevated plus maze task. In contrast, there are no synergistic effects between WiFi signal and restraint stress on the brain.

Effects of prenatal exposure to WIFI signal (2.45GHz) on postnatal development and behavior in rat: Influence of maternal restraint.

The present study was carried out to investigate the potential combined influence of maternal restraint stress and 2.45GHz WiFi signal exposure on postnatal development and behavior in the offspring of exposed rats. 24 pregnant albino Wistar rats were randomly assigned to four groups: Control, WiFi-exposed, restrained and both WiFi-exposed and restrained groups. Each of WiFi exposure and restraint occurred 2h/day along gestation till parturition. The pups were evaluated for physical development and neuromotor maturation. Moreover, elevated plus maze test, open field activity and stationary beam test were also determined on postnatal days 28, 30 and 31, respectively. After behavioral tests, the rats were anesthetized and their brains were removed for biochemical analysis. Our main findings showed no detrimental effects on gestation progress and outcomes at delivery in all groups. Subsequently, WiFi and restraint, per se and mainly in concert altered physical development of pups with slight differences between genders. Behaviorally, the gestational WiFi irradiation, restraint and especially the associated treatment affected the neuromotor maturation mainly in male progeny. At adult age, we noticed anxiety, motor deficit and exploratory behavior impairment in male offspring co-exposed to WiFi radiation and restraint, and in female progeny subjected to three treatments. The biochemical investigation showed that, all three treatments produced global oxidative stress in brain of both sexes. As for serum biochemistry, phosphorus, magnesium, glucose, triglycerides and calcium levels were disrupted. Taken together, prenatal WiFi radiation and restraint, alone and combined, provoked several behavioral and biochemical impairments at both juvenile and adult age of the offspring.

Subacute static magnetic field exposure in rat induces a pseudoanemia status with increase in MCT4 and Glut4 proteins in glycolytic muscle.

The purpose of this study was to investigate the effect of subacute exposure to static magnetic fields (SMF) on hematological and muscle biochemical parameters in rats. Male Wistar rats, daily exposed to SMF, were exposed to SMF (128 mT, 1 h/day) during 15 consecutive days. SMF-exposed rats showed a significant decrease in red blood cell (RBC) count, hemoglobin (Hb), and hematocrit (Ht) values compared to sham-exposed rats (p < 0.05). Concomitant decreases of plasma iron level against increase in transferrin amount were also observed after SMF exposure (p < 0.0.05). In postprandial condition, SMF-exposed rats presented higher plasma lactate (p < 0.01). Additionally, SMF exposure increased monocarboxylate transporters (MCT4) and glucose transporter 4 (Glut4)'s contents only in glycolytic muscle (p < 0.05). SMF exposure induced alteration of hematological parameters; importantly, we noticed a pseudoanemia status, which seems to affect tissue oxygen delivery. Additionally, SMF exposure seems to favor the extrusion of lactate from the cell to the blood compartment. Given that, these arguments advocate for an adaptive response to a hypoxia status following SMF exposure.

Effects of combined ferrous sulfate administration and exposure to static magnetic field on brain oxidative stress and emotional behavior.

The present study was done to investigate behavioral effects and oxidative stress in iron- treated and co-exposed static magnetic field (SMF)-iron rats. Anxiety in the elevated plus- maze test, and motor skills were also assessed in the stationary beam and suspended string tests. After behavioral tests, the rats were anesthetized and their brains were removed for biochemical analysis. The co-exposure to iron and SMF induced a significant difference in elevated plus-maze test in rats. The frequency of entries and time spent in the open arms was significantly reduced (p<0.05) in the iron- and SMF-exposed group compared with the group treated with iron alone and in the control group. However, no significant difference was noticed for the motor skill test between the three groups. The biochemical investigation showed that malondialdehyde level increased (p<0.001) and that glutathione level and catalase enzyme activity decreased (p<0.001) in brain of iron- and SMF-exposed group. The dose of iron alone used in present study, was unable to induce any effect. However, the 128 mT SMF in the presence of iron ions in the body can induce disruption in the emotional behavior and can produce oxidative stress in brain tissue of rats.

Static magnetic field exposure-induced oxidative response and caspase-independent apoptosis in rat liver: effect of selenium and vitamin E supplementations.

In the present study, we investigated the implication of oxidative stress and apoptosis under static magnetic field (SMF) in the brain and liver. Moreover, we estimated the protective role of selenium and vitamin E in rat tissues against disorders induced by SMF. Exposure of rats to SMF (128 mT, 1 h/day during five consecutive days) increased the activity of catalase (CAT) (+24 %) in the liver but not in the brain. By contrast, the same treatment failed to alter malondialdehyde (MDA) concentration in the brain and liver. Exposure to SMF also induced hepatocyte apoptosis through a caspase-independent pathway involving mitochondrial apoptosis-inducing factor (AIF) but not in the brain. Selenium and vitamin E supplementations to SMF-exposed rats restored liver CAT activity but failed to minimize liver apoptosis.

Does static magnetic field-exposure induced oxidative stress and apoptosis in rat kidney and muscle? Effect of vitamin E and selenium supplementations.

Static magnetic fields (SMFs) effect observed with radical pair recombination is one of the well-known mechanisms by which SMFs interact with biological systems. Our aim was to study whether SMF induces oxidative stress and apoptosis in rat tissues and to evaluate the possible protector effect of selenium (Se) and vitamin E (vit E) supplementations. Rats were randomly divided into control, SMF-exposed, Se-treated, vit E-treated, SMF exposed rats and co-treated with Se, and SMF exposed rats and co-treated with vit E. After animal sacrifice, catalase (CAT) activity and malondialdehyde (MDA) concentration were measured and apoptosis inducing factor (AIF) immunohistochemical labeling was performed in kidney and muscle. Exposure of rats to SMF (128 mT, 1 h/day for 5 days) increased the MDA concentrations (+25%) and CAT activities (+34%) in kidney but not in muscle. By contrast, the same treatment failed to induce a caspase-independent pathway apoptosis in both tissues. Interestingly, Se pre-treatment inhibited the increase of MDA concentrations and CAT activities in kidney in SMF-exposed rats. However, vit E administration corrected only MDA levels in rat kidney. In conclusion, exposure to SMF induced oxidative stress in kidney that can be prevented by treatment with Se or vit E.

Involvement of autonomic nervous activity changes in gastroesophageal reflux in neonates during sleep and wakefulness.

BACKGROUND: It has been suggested that disturbed activity of the autonomic nervous system is one of the factors involved in gastroesophageal reflux (GER) in adults. We sought to establish whether transient ANS dysfunction (as assessed by heart rate variability) is associated with the occurrence of GER events in neonates during sleep and wakefulness. METHODS: Nineteen neonates with suspected GER underwent simultaneous, synchronized 12-hour polysomnography and esophageal multichannel impedance-pH monitoring. We compared changes in HRV parameters during three types of periods (control and prior to and during reflux) with respect to the vigilance state. RESULTS: The vigilance state influenced the distribution of GER events (P<0.001), with 53.4% observed during wakefulness, 37.6% observed during active sleep and only 9% observed during quiet sleep. A significant increase in the sympathovagal ratio (+32%, P=0.013) was observed in the period immediately prior to reflux (due to a 15% reduction in parasympathetic activity (P=0.017)), relative to the control period. This phenomenon was observed during both wakefulness and active sleep. CONCLUSION: Our results showed that GER events were preceded by a vigilance-state-independent decrease in parasympathetic tone. This suggests that a pre-reflux change in ANS activity is one of the factors contributing to the mechanism of reflux in neonates.

Effects of combined ferrous sulphate administration and exposure to static magnetic field on spatial learning and motor abilities in rats.

PRIMARY OBJECTIVE: Occupational exposure to static magnetic fields (SMF) increases, in particular due to the widespread use of Magnetic Resonance Imaging (MRI) for medical diagnosis, thus raising health concerns. This study investigated the behavioural effects of 128 mT SMF in rats and examined the hypothesis that iron supplementation (3 mg kg(-1) for 5 days) potentiate the effects of SMF. METHODS: Spatial learning abilities in the water maze, motor co-ordination in the rotarod and motor skills in the stationary beam and suspending string tests were assessed in iron-treated, SMF-exposed and co-exposed SMF-iron rats. RESULTS: Acquisition of the water maze navigation task was unaffected in all groups. SMF-exposed and iron-treated rats showed a deficit in the 7-day retention test. No deficit was found in the rotarod and suspended string tests in all groups. Only iron-treated rats were impaired in the stationary beam test. A combination of iron and SMF treatments did not produce additional degradation of performance in all tests. CONCLUSION: SMF exposure had no massive effect but affected long-term spatial memory. Iron supplementation and 128 mT SMF had no synergistic effects.

Relationship between sleep and acid gastro-oesophageal reflux in neonates.

The aim of the present study was to investigate the impact of gastro-oesophageal acid reflux on sleep in neonates and, reciprocally, the influence of wakefulness (W) and sleep stages on the characteristics of the reflux (including the retrograde bolus migration of oesophageal acid contents). The pH and multichannel intraluminal impedance were measured during nocturnal polysomnography in 25 infants hospitalised for suspicion of gastro-oesophageal reflux. Two groups were constituted according to whether or not the infants displayed gastro-oesophageal reflux (i.e. a reflux group and a control group). There were no differences between the reflux and control groups in terms of sleep duration, sleep structure and sleep state change frequency. Vigilance states significantly influenced the gastro-oesophageal reflux pattern: the occurrence of gastro-oesophageal reflux episodes was greater during W (59 ± 32%) and active sleep (AS; 35 ± 30%) than during quiet sleep (QS; 6 ± 11%), whereas the mean duration of gastro-oesophageal reflux episodes was higher in QS than in W and AS. The percentage of retrograde bolus migrations of distal oesophageal acid content was significantly higher in AS (62 ± 26%) than in W (42 ± 26%) and QS (4.5 ± 9%). In neonates, gastro-oesophageal reflux occurred more frequently during W, whereas the physiological changes associated with sleep state increase the physiopathological impact of the gastro-oesophageal reflux. The duration of oesophagus-acid contact was greater during sleep; AS facilitated the retrograde migration of oesophageal acid content, and QS was characterised by the risk of prolonged acid mucosal contact.

Effects of exposure to static magnetic field on motor skills and iron levels in plasma and brain of rats.

PRIMARY OBJECTIVE: The present work investigated the behavioural and biochemistry effects of moderate exposure to a static magnetic field (SMF) in rats. SMF effects were evaluated in sham- and SMF-exposed rats. METHODS: Adult Wistar rats were exposed for 1 hour per day for 5 consecutive days to 128 millitesla (mT) SMF. Then, their motor skills were tested using a Stationary beam and Suspended string test. Iron level in plasma and brain (i.e. frontal cortex, basal ganglia, hippocampus and cerebellum) was measured. RESULTS: No significant change was observed between sham and SMF-exposed rats in the Stationary beam and Suspended string test. However, the same treatment induced an increase in plasma transferrin content (+25.4%) and decreased the iron level in plasma (-16.2%). The SMF treatment failed to alter the iron concentration in the brain. CONCLUSION: The findings indicate that SMF exposure induced iron deficiency in plasma but did not induce motor-skills deficit.

Are benzo[a]pyrene-DNA adducts an accurate biomarker of long-term in utero exposure to smoking?

BACKGROUND: Maternal smoking during pregnancy is associated with adverse perinatal outcomes. In view of concerns about underreporting, benzo[a]pyrene (B[a]P)-DNA adducts could be used to provide information about long-term in utero exposure to smoking but have not previously been used with samples from neonates. This study aimed to verify whether B[a]P-DNA adducts could accurately assess tobacco smoke exposure during fetal life. The objectives were to correlate B[a]P-DNA adduct levels with active maternal and passive smoking and to determine the sensitivity and specificity of smoking and nonsmoking status by comparing neonatal B[a]P-DNA adduct levels with those of maternal self-reports. MATERIALS AND METHODS: B[a]P-DNA adducts in neonatal buccal cell samples were determined by a competitive immunoassay. Three groups of neonates were constituted according to maternal self-reported smoking status during pregnancy: nonsmokers (n=25; control group), <10 cigarettes per day (n=18; S- group), or >10 cigarettes per day (n=21; S+ group). RESULTS: The mean B[a]P-DNA adduct level rose significantly when comparing the controls with the S- and S+ groups. Maternal active smoking had the strongest effect on B[a]P-DNA adduct levels in neonates. A cross analysis between B[a]P-DNA adduct levels and maternal self-reported levels revealed high sensitivity and specificity. CONCLUSIONS: This preliminary study suggests that B[a]P-DNA adducts are reliable biomarkers for the screening of long-term in utero exposure to smoking and are accurate when compared with maternal self-reported levels of active smoking. Detection of B[a]P-DNA adducts in neonates could provide a useful, noninvasive tool in clinical risk assessment studies but would benefit from further confirmation with another validated biomarker.