OBJECTIVETo explore the effect of dibutyl phthalate (DBP) on the biochemical enzymes and lipid peroxidation in rats.

METHODSHealthy 6-week old male Sprague-Dawley rats were randomly divided into 4 groups with 16 in each. DBP dissolved in peanut oil was administered by gavage at dosages of 0, 250, 500 and 1000 mg/(kg x d). After 2- and 4-week DBP exposure, 8 rats in each group were killed, with certain organs selected and weighed. The activities of biochemical enzymes and glutathione peroxidase (GSH-Px) and the levels of glutathione (GSH) in the serum and testis homogenate were determined respectively.

RESULTSDBP induced a rise in the liver organ body weight ratio, but a fall in the testis organ body weight ratio, and it was significant in the highest exposure group compared with the control after either 2-week or 4-week treatment (P < 0.01). After 2-week DBP exposure, GSHPx activities in the serum and GSH levels in the testis homogenate showed a decreasing tendency, but GSHPx activities increased markedly in the testis homogenate (P < 0.05). After 4-week DBP exposure, while alkaline phosphatase (ALP) activities in the serum revealed an increasing tendency, sorbitol dehydrogenase (SDH) activities were inhibited significantly in both the serum and the testis homogenate at the dosage of 1000 mg/(kg x d) compared with the control group (P < 0.01). Furthermore, GSH contents in the serum were also affected at this dose (P < 0.05).

CONCLUSIONThe results indicate that DBP administration strongly affects the liver and the testis organ body weight ratios. Lipid peroxidation is one possible toxic mechanism caused by DBP. SDH may be one of the most sensitive toxic indices when exposed to DBP.

Alkaline Phosphatase ; metabolism ; Animals ; Dibutyl Phthalate ; toxicity ; Dose-Response Relationship, Drug ; Glutathione ; metabolism ; L-Iditol 2-Dehydrogenase ; metabolism ; Lipid Peroxidation ; drug effects ; Male ; Random Allocation ; Rats ; Rats, Sprague-Dawley ; Testis ; drug effects ; metabolism

OBJECTIVETo explore the effects of glucose concentration fluctuation on function of cultured bovine arterial endothelial cells and underlying mechanism.

METHODSThe thoracic aorta of newborn calf was used for primary endothelial cells culture. Cells were divided into 3 groups and cultured for 48 h: control group (C, 5.5 mmol/L), constant high glucose group (HG, 30 mmol/L) and glucose fluctuation (GF, three circles of 2 h 30 mmol/L followed by 3 h 5.5 mmol/L, 30 mmol/L overnight, repeat the whole procedure on the following day) groups. The membranes fluidity of endothelial cells was detected by fluorescence polarization method. The contents of sorbierite, aldose reductase (AR), sorbitol dehydrogenase (SDH) and advanced glycation end products (AGEs) were measured. RAGE, eNOS and ET-1 mRNA expressions were detected by semi-quantitative RT-PCR.

RESULTSThe membranes fluidity of endothelial cells in HG or GF group were significantly decreased compared with the control group (all P < 0.01) and significantly lower in GF group than those in HG group (all P < 0.01). Sorbierite, AR and AGEs concentrations were significantly higher in HG and GF groups than those in control group (all P < 0.01) and AR and AGEs concentrations were significantly higher in GF group than that in HG group (all P < 0.01). SDH of endothelial cells in HG or GF group were decreased compared with the control group and lower in GF group than in HG group (all P < 0.05). In addition, the mRNA levels of RAGE, eNOS and ET-1 were significantly upregulated compared with the control group (all P < 0.01).

CONCLUSIONSGlucose concentration fluctuation can result in more severe bovine arterial endothelial cells dysfunction than high glucose via activating polyols metabolic pathways, upregulating the expression of AGEs, eNOS and ET-1. Therefore, glucose concentration fluctuation might play a crucial role on macrovascular complications of diabetes.

Aldehyde Reductase ; analysis ; Animals ; Aorta, Thoracic ; cytology ; Cattle ; Cells, Cultured ; Endothelial Cells ; metabolism ; pathology ; Endothelin-1 ; analysis ; Endothelium, Vascular ; cytology ; metabolism ; Glucose ; metabolism ; Glycation End Products, Advanced ; analysis ; L-Iditol 2-Dehydrogenase ; analysis ; Membrane Fluidity ; Nitric Oxide Synthase Type III ; analysis

BACKGROUND: Exposure to the ionizing radiation (IR) encountered outside the magnetic field of the Earth poses a persistent threat to the reproductive functions of astronauts. The potential effects of space IR on the circadian rhythms of male reproductive functions have not been well characterized so far. METHODS: Here, we investigated the circadian effects of IR exposure (3 Gy X-rays) on reproductive functional markers in mouse testicular tissue and epididymis at regular intervals over a 24-h day. For each animal, epididymis was tested for sperm motility, and the testis tissue was used for daily sperm production (DSP), testosterone levels, and activities of testicular enzymes (glucose-6-phosphate dehydrogenase (G6PDH), sorbitol dehydrogenase (SDH), lactic dehydrogenase (LDH), and acid phosphatase (ACP)), and the clock genes mRNA expression such as Clock, Bmal1, Ror-α, Ror-β, or Ror-γ. RESULTS: Mice exposed to IR exhibited a disruption in circadian rhythms of reproductive markers, as indicated by decreased sperm motility, increased daily sperm production (DSP), and reduced activities of testis enzymes such as G6PDH, SDH, LDH, and ACP. Moreover, IR exposure also decreased mRNA expression of five clock genes (Clock, Bmal1, Ror-α, Ror-β, or Ror-γ) in testis, with alteration in the rhythm parameters. CONCLUSION These findings suggested potential health effects of IR exposure on reproductive functions of male astronauts, in terms of both the daily overall level as well as the circadian rhythmicity.
ARNTL Transcription Factors/genetics* ; Acid Phosphatase ; Animals ; CLOCK Proteins/genetics* ; Circadian Rhythm/radiation effects* ; Epididymis/radiation effects* ; Gene Expression/radiation effects* ; Genitalia, Male/radiation effects* ; Glucosephosphate Dehydrogenase ; L-Iditol 2-Dehydrogenase ; L-Lactate Dehydrogenase ; Male ; Mice ; Mice, Inbred C57BL ; Models, Animal ; Nuclear Receptor Subfamily 1, Group F, Member 1/genetics* ; Nuclear Receptor Subfamily 1, Group F, Member 2/genetics* ; Nuclear Receptor Subfamily 1, Group F, Member 3/genetics* ; RNA, Messenger/genetics* ; Radiation Exposure ; Radiation, Ionizing ; Reproductive Physiological Phenomena/radiation effects* ; Sperm Motility/radiation effects* ; Spermatozoa/radiation effects* ; Testis/radiation effects*