OBJECTIVETo explore the influence of nonylphenol (NP) on the neural behavioral development of filial generation rats exposed via placenta.

METHODSOn the first day of the pregnancy, the SD rats were divided into four groups, and orally administered with NP at doses of 0, 50, 100 and 200 mg/kg on gestational day 9 approximately 15 respectively. The offspring rats of each groups were examined to observe the impact of NP on the early physiological, neurobehavioral development. The changes of filial generation body weight (from generation day 1 to 28) were measured. Brain tissues were stained with Hematoxylin-eosin and Congo red to observe with optical microscope.

RESULTSIn contrast to the control group, the early physiological markers (pinna detachment, hair growth, tooth growth and eye opening) and the early neurobehavioral development indices (surface righting, air righting, acoustic startle and visual placing) were significantly delayed in the groups of NP 200mg/kg dose (P < 0.05). The developing time of physiological markers decreased from (4.5 +/- 0.8, 5.2 +/- 0.8, 12.7 +/- 1.4, 16.0 +/- 1.7) d to (3.6 +/- 0.5, 3.6 +/- 0.5, 11.1 +/- 1.1, 12.7 +/- 1.3) d while neurobehavioral developing time decreased from (6.5 +/- 0.8, 11.3 +/- 0.5, 11.2 +/- 1.0, 20.2 +/- 1.0) d to (5.1 +/- 0.4, 8.3 +/- 0.5, 9.3 +/- 0.5, 9.3 +/- 0.5) d (P < 0.05 or P < 0.01). The body weights of filial generation rats were decreased obviously from 1 st day to 28th day. Histopathological examination displayed that hippocampal neurons had congestion and oedema in the group of 100, 200 mg/kg dose.

CONCLUSIONExposures to NP during gestation might impair the neurobehavioral development of F1 rats significantly.

Animals ; Female ; Hippocampus ; pathology ; Phenols ; toxicity ; Placenta ; drug effects ; Pregnancy ; Prenatal Exposure Delayed Effects ; physiopathology ; Rats ; Rats, Sprague-Dawley

OBJECTIVETo identify the mutation of Cu/Zn superoxide dismutase(SOD1) gene in an amyotrophic lateral sclerosis (ALS) family with unique phenotype.

METHODSFive exons of SOD1 gene were amplified by PCR. The differences of these products were analyzed by PCR-single strand conformation polymorphism and visualized by silver staining.

RESULTSAbnormal bands were found in exons 2 and 5 of SOD1 gene in several familial members. DNA sequence analysis verified that a base pair insertion occurred in the codon area of exon 2 and in the intron area of exon 5. And the insertion mutation of exon 2 led to a frameshift mutation and premature stop. It is a new type of SOD1 mutation which may be associated with familial amyotrophic lateral sclerosis.

CONCLUSIONInsertion mutation of exon 2 may be responsible for the disease of an ALS family in Chongqing.

Adult ; Amyotrophic Lateral Sclerosis ; genetics ; Humans ; Mutation ; Polymorphism, Single-Stranded Conformational ; Superoxide Dismutase ; genetics ; Superoxide Dismutase-1

Membrane-type 1 matrix metalloproteinase (MT1 MMP/MMP 14) plays crucial roles in tumor cell growth, invasion, and angiogenesis. To clarify whether the endogenously expressed MT1-MMP in metastatic human ovarian carcinoma cell lines SKOV3 plays a critical role in tumor cell invasiveness, antisense MT1-MMP cloned in eukaryotic expression vector pMMP14as was transferred into SKOV3 cells. 48h after transfection, decreased expression of endogenous MT1-MMP protein was detected in pMMP14as transfected SKOV3 cells and the activation of pro MMP2was inhibited markedly. The mean percentage of invasive cells was (62. 50 ±5. 30) % in pMMP14as-transfected cells, which was obviously less than that (97.20±6.90) % in the control.Thus, antisense MT1 MMP effectively inhibited the endogenous MT1 MMP expression and the invasiveness in SKOV3 cells, suggesting that MT1-MMP may be a therapeutic target molecule for human invasive ovarian cancers.