2,4-Dichlorophenoxyacetic acid effects on nephrotoxicity in rats during late pregnancy and early postnatal periods

2,4-Dichlorophenoxyacetic acid (2,4-D) is largely used as a selective herbicide in Tunisia. The purpose of this study was to investigate the effects of 2,4-D on the kidneys of adult rats and their suckling pups. Female Wistar rats were divided into two groups: the controls and the treated rats that received 600 mg/L of 2,4-D in their drinking water from the 14th day of pregnancy until day 14 after delivery.Exposure to 2,4-D induced nephrotoxicity as evidenced by an increase in thiobarbituric acid reactive substances and protein carbonyl levels and a decrease in antioxidant enzyme activities such as catalase, superoxide dismutase, glutathione peroxidase in the kidneys of suckling pups and their mothers. In addition, a significant decline in kidney glutathione, non-protein thiol and vitamin C levels was also observed.Histological changes, seen in the kidney of mothers and their pups treated with 2,4-D are characterized by a narrowed Bowman’s space, tubular epithelial cells degeneration, widened tubular lumen and vascular congestion.     

Pigmented lesion in the inguinal region

Pigmented Bowen disease (PBD) is a rare tumor characterized by increased melanin pigment in the epidermis or papillary dermis in addition to the typical findings of Bowen disease. We report the case of a 60-year-old woman who presented with a 6-month history of a gradually enlarging solitary dark brown plaque in her right inguinal region. Histopathology showed hyperkeratosis with parakeratosis, acanthosis, disorganization of epidermal architecture, atypical keratinocytes, and increased melanin pigment of the papillary dermis. Considering the clinical and the histological evidence, a diagnosis of PBD was established. Complete resection confirmed the diagnosis. Pigmented Bowen disease is an unusual form of squamous carcinoma in situ. Other tumors in the differential diagnosis include pigmented basal cell carcinoma and superficial spreading melanoma.     

Moderate phenotypic expression of familial hypercholesterolemia in Tunisia

BackgroundAutosomal Dominant Hypercholesterolemia (ADH) is an autosomal dominant disease caused by mutations in the low density lipoprotein receptor (LDLR), apolipoprotein B (APOB), and proprotein convertase subtilisin/kexin type 9 (PCSK9) genes. Xanthomas and coronary heart diseases (CHD) at an early age are the major clinical manifestations of the disease.Methods16 families with familial hypercholesterolemia from different regions in Tunisia participated in the study. Mutations within the LDLR gene were screened through DNA sequencing. Lipids values were measured by standard enzymatic methods.ResultsWe present here thirty five homozygotes and fifty six heterozygotes. Homozygotes presented extensive xanthomatosis, variable clinical manifestations of CHD, and total cholesterol levels in males and females of 17.26 ± 4.18 and 17.64 ± 2.59 mmol/L respectively. HDL-cholesterol levels were 0.62 ± 0.24 and 1.00 ± 0.61 mmol/L for males and females, respectively. None of the heterozygotes had tendon xanthomas (except for one female aged 62), eight had corneal arcus, and nine developed CHD mean between 46 and 88 years old. Total cholesterol levels in males and females ranged from 4.60 to 8.90 and from 4.30 to 10.50 mmol/L, respectively.ConclusionTunisian FH heterozygotes are characterized by a moderate clinical and biological expression of the disease.     

Refractory epilepsy in PSEN 1 mutation (I83T)

ABSTRACT

Mutations in the presenilin-1 gene (PSEN1) on chromosome 14 are the most common cause of autosomal dominant Alzheimer's disease (ADAD), which has a broad clinical phenotype, encompassing not only dementia but a variety of other neurological features. We report the case of a 32 years old man with a family history of early onset AD associated with a PSEN1 mutation in the exon 4 (I83T). The proband’s, carrying the mutation, present a refractory epilepsy predating cognitive decline. We discuss the physiopathological mechanisms of epilepsy during AD associated with PSEN 1 mutation, the possibility of linking this epilepsy to the mutation?.     

Bone mineral density of young boy soccer players at different pubertal stages: relationships with hormonal concentration

ObjectivesTo examine the effects of soccer in relation with the hormonal concentration, on the bone mass of young Tunisian players at different pubertal stages.MethodsTwo groups of 152 young boys (age: 13.3 ± 0.9 years) participated in this study: (1) 91 soccer players, and (2) 61 non-athletic boys used as control subjects. The bone mineral density (BMD) and the bone mineral content (BMC) were measured by dual-energy X-ray absorptiometry (DXA). Pubertal stages were assessed, and serum concentrations of insulin-like growth factor-1 (IGF-1), insulin-like growth factor binding protein-3 (IGFBP-3), growth hormone (GH) and the total testosterone were measured.ResultsThe BMD and BMC for whole body, lumbar spine, femoral neck, pelvis and lower limbs were higher in soccer players than in controls (p < 0.001). In early puberty, the soccer players also exhibited significantly greater BMD and BMC in the whole body and in weight-bearing bones compared with the controls (p < 0.001). However, there was no intersubject variability due to puberty in either BMD or BMC. The pubescent soccer players had significantly higher hormonal concentrations of IGF-1 and IGFBP-3 than their counterpart controls (p < 0.05). Moreover, the whole body BMD was significantly (p < 0.001) correlated with GH, IGF-1 and IGFBP-3 but not with the testosterone concentrations.ConclusionThe soccer participation of boys is generally associated with the improvement of their bone mass which is mainly marked at early and late puberty. The relationships between somatotropic axis hormones and BMD of the players may be linked to the parallel development of these two parameters during puberty.     

Dimethoate-induced oxidative damage in erythrocytes of female adult rats: possible protective effect of vitamin E and selenium supplemented to diet

Pesticide hazards have been accentuated by the sharp rise in their agricultural, industrial and domestic use. Acute exposure to pesticides can cause oxidative damage. Our study investigated the potential ability of selenium (Se) and/or vitamin E, used as nutritional supplements, to alleviate erythrocyte oxidative damage induced by dimethoate (DM), an organophosphate pesticide. Female Wistar rats were exposed to DM (0.2g/L(-1) of drinking water), DM + Se (0.5 mg/kg of diet), DM + vitamin E (100 mg/kg of diet), or DM + Se + vitamin E. Rats exposed to DM for 30 days showed an increase in malondialdehyde levels, superoxide dismutase and glutathione peroxidase activities in their erythocytes, while Na(+),K(+)-ATPase and catalase activities, glutathione, non-protein thiol, vitamin E and vitamin C levels decreased. We also noted an increase in lactate dehydrogenase activity, marker of haemolysis and a decrease in acetylcholinesterase, the principal mode of organophosphorus action. Co-administration of Se or vitamin E to the diet of DM-treated rats ameliorated the biochemical parameters cited above. But the combined effect of Se and vitamin E was more powerful in antagonizing DM-induced oxidative stress. Therefore, our investigation revealed that both Se and vitamin E were useful elements in preventing DM-induced erythrocytes damage.