Unilateral biportal endoscopic discectomy (UBE) versus percutaneous endoscopic lumbar discectomy (PELD) in the treatment of lumbar disc herniation linked with posterior ring apophysis separation: a retrospective study.

OBJECTIVES: Posterior ring apophysis separation (PRAS) associated with lumbar disc herniation (LDH) is a relatively rare form of disc herniation. This study aims to evaluate the clinical effectiveness of unilateral biportal endoscopic discectomy (UBE) and percutaneous endoscopic lumbar discectomy (PELD) in the treatment of PRAS with LDH. METHODS: We enrolled 41 patients who met the inclusion criteria to undergo either unilateral biportal endoscopic discectomy (UBE) (15 cases) or percutaneous endoscopic lumbar discectomy (PELD) (26 cases) between October 2022 and October 2023. Perioperative evaluation parameters included mean operative time, hemoglobin (Hb) loss, length of stay (LOS), and postoperative complications. Outcomes were assessed at admission, as well as at 1, 3, and 6 months post-surgery using the Visual Analog Scale (VAS) and the Oswestry Disability Index (ODI). Additionally, we evaluated the results according to the modified MacNab criteria. RESULTS: Both groups demonstrated improvements in postoperative VAS and ODI scores. However, there were no significant differences between the two groups in VAS and ODI scores before surgery, or at 1, 3, and 6 months post-surgery. Additionally, no notable differences were observed in the modified MacNab criteria. The UBE group experienced greater hemoglobin (Hb) loss, longer mean operative time, and increased length of stay (LOS) compared to the PELD group. Furthermore, two patients in the PELD group reported recurrence, while one patient in the UBE group experienced a dural tear. CONCLUSIONS: UBE and PELD possess strong clinical effectiveness for treating PRAS with LDH. Although the UBE group had a longer mean operative time and LOS, with more Hb loss, the UBE group had a lower recurrence rate. Therefore, UBE remains safe and innovative for the treatment of PRAS with LDH.

[Roles of CYP2E1 in liver damage induced by 1,2-dichloroethane].

OBJECTIVE: To explore the expression of CYP2E1 in the liver of mice and its effects on liver injury induced by 1,2-dichloroethane (1, 2-DCE). METHODS: (1) Thirty-two female mice were randomly divided into four groups, which were control group, low dose group, medium dose group and high dose group. Mice were exposed to 1,2-DCE through respiratory for 4 h per day for 10 days. At the end of exposure, the mice were sacrificed, their blood and liver were collected rapidly. Pathological analysis was examined. Activity of ALT and AST in serum and activity of CYP2E1 in liver were mice were randomly divided into six groups, ie simple control group, corn oil control group, inhibitor control group, simple poisonous group, low and high dose diallyl sulfide (DAS) intervention groups. Mice were treated orally with DAS in corn oil 4 hours before 1, 2-DCE exposure. The examination indicators were as aforementioned. RESULTS: (1) Compared to control group, activity of ALT in serum of mice in the high dose group and expression of CYP2E1 in the liver of mice in medium and high dose group increased significantly. In addition, the histological observation suggested obvious liver damage in medium and high dose group. (2) CYP2E1 protein expression and activity in liver and ALT in serum decreased significantly in DAS-intervention groups compared to simple poisonous group. Along with the changes of CYP2E1 and ALT, pathological changes of liver damage was better. CONCLUSION: Our results suggested that expression of CYP2E1 and oxidative damage in the liver could be induced by 1,2-DCE exposure, and CYP2E1 inhibitors can reduce the hepatic tissue damage caused by DCE.

Roles of CYP2e1 in 1,2-dichloroethane-induced liver damage in mice.

The aim of this study was to explore the roles of cytochrome P450 2E1 (CYP2E1) in 1,2-dichloroethane (1,2-DCE)-induced liver damage. Two parts were included in this study: first, effect of 1,2-DCE on microsomal expression of CYP2E1, and second, potential of an inhibitor of CYP2E1 to reduce 1,2-DCE-induced liver damage. In part one, mice were exposed to 0, 0.225, 0.45, or 0.9 g/m3 1,2-DCE for 10 days, 3.5 h per day through static inhalation. In part two, mice were divided into blank control, solvent control, inhibitor control, 1,2-DCE-poisoned group, and low or high intervention group. In part one, compared to the control, serum alanine aminotransferase (ALT) activities and hepatic malondialdehyde (MDA) levels in 0.9 g/m3 1,2-DCE group, and microsomal CYP2E1 protein expression and activity in both 0.45 and 0.9 g/m3 1,2-DCE groups increased significantly; conversely, hepatic nonprotein sulfhydryl (NPSH) levels in both 0.45 and 0.9 g/m3 1,2-DCE groups and hepatic SOD activities in 0.9 g/m3 1,2-DCE group decreased significantly. In part two, microsomal CYP2E1 protein expression and activity decreased significantly in both low and high intervention groups compared to 1,2-DCE-poisoned group. Along with the changes of CYP2E1, hepatic MDA levels and serum ALT activities decreased; conversely, hepatic NPSH levels and SOD activities increased significantly in high intervention group. Taken together, our results suggested that 1,2-DCE could enhance CYP2E1 protein expression and enzymatic activity, which could cause oxidative damage in liver, serving as an important mechanism underlying 1,2-DCE-induced liver damage. © 2015 Wiley Periodicals, Inc. Environ Toxicol 31: 1430-1438, 2016.

Roles of aquaporins and matrix metalloproteinases in mouse brain edema formation induced by subacute exposure to 1,2-dichloroethane.

The aim of this study was to explore the effects of 1,2-dichloroethane (1,2-DCE) on expression of aquaporins (AQPs) and matrix metalloproteinases (MMPs) in the process of brain edema formation. Two parts were included in this study, establishment of animal model of brain edema, and mechanism of brain edema induced by subacute exposure to 1,2-DCE. In part one, mice were exposed to 0, 1.1, 1.2 or 1.3g/m(3) 1,2-DCE, 3.5h per day for 3days. Pathological analysis and water content detection in the brain were examined. In part two, mice were exposed to 1.2g/m(3) 1,2-DCE, 3.5h per day for 1, 2 or 3days, named group D, E and F, respectively. Expression of AQP4, MMP2 and MMP9 in the brain was determined by immunochemical staining, western blot and real time PCR. According to the results of part one, the 1.2g/m(3) dose was chosen for part two, a follow-up time-course study. In part two, protein expression of MMP2 and MMP9 in group F, and AQP4 in group E and F significantly increased compared to the control. Similarly, mRNA levels of AQP4 in group F, and MMP9 in group E and F significantly increased. Our results suggested that exposure to 1,2-DCE might up-regulate the expression of AQP4 protein and MMP9 mRNA at the early phase of brain edema, and AQP4 may play an important role in the brain edema formation.

Comparison of speciated arsenic levels in the liver and brain of mice between arsenate and arsenite exposure at the early life.

The aim of this study was to compare the risk from exposure to arsenate (iAs(V) ) or arsenite (iAs(III) ) at the early life. Mother mice were exposed to equimolar dose of iAs(V) and iAs(III) via drinking water during gestation and lactation. Their offspring continually drank the same water after weaning. Levels of speciated arsenic in both liver and brain were analyzed by hydride generation of volatile arsines and atomic absorption spectrophotometry (HG-AAS). In the liver, inorganic arsenic (iAs) levels significantly increased from postnatal day (PND) 15, and those on PND 35 were significantly higher than on PND 15 and 21 in iAs(III) exposed mice, but iAs levels did not significantly differ until PND 35 in iAs(V) exposed mice; Furthermore, all speciated arsenic levels on PND 35 and dimethylarsinic acid (DMA) levels on PND 1 were significantly higher in iAs(III) exposed mice than those in iAs(V) exposed mice. In the brain, iAs levels increased significantly on PND 21, but those declined sharply on PND 35 in either iAs(III) or iAs(V) exposed mice, however the mean difference between the two exposure groups was not significant; whereas DMA levels in iAs(III) exposed mice were significantly higher than those in iAs(V) exposed mice on both PND 1 and 35. In conclusion, findings from this study suggested that iAs(III) was preferentially accumulated into liver, and expected to result in more efficient methylation capacity than iAs(V) ; either iAs(V) or iAs(III) might be accumulated in the brain readily, when immature blood brain barrier can not limit it into brain. Hence, exposure to either iAs(V) or iAs(III) at the early life may increase the risk of iAs exposure in the brain.

Prolonged environmental exposure of arsenic through drinking water on the risk of hypertension and type 2 diabetes.

Prolonged exposure to inorganic arsenic has been a severe environmental public health issue worldwide in the recent decades. Increasing evidence has suggested a possible role of prolonged arsenic exposure through drinking water in the development of arsenic-induced chronic noncancer diseases, among which hypertension and type 2 diabetes (T2D) are the focus of concern. Although exposure to high levels of arsenic has been reported to be associated with excess risk of hypertension or T2D in a dose-dependent manner, the association has yet to be established, especially low-level exposure. This cross-sectional study was designed to evaluate the potential association between prolonged environmental arsenic exposure through drinking water and the prevalence of hypertension and T2D in Inner Mongolia, China, with emphasis on the assessment of low-level exposure. In this study (a total of 669 men and women), we found that the blood pressure levels were significantly correlated with cumulative arsenic exposure and that the systolic blood pressure of the subjects with arsenic exposure>50 µg/L was significantly higher than those of the subjects with <10 and 10-50 µg/L exposure. Significant prevalence of hypertension was found in the subjects of the >50 µg/L group both before and after adjustment for confounders. In addition, a significant negative relationship was found between urinary arsenic percentage of dimethylated arsenic (DMA%) and the prevalence of hypertension in the >50 µg/L group. However, low-level arsenic exposure (10-50 µg/L) was not statistically associated with hypertension. No significant difference of blood glucose was found among the groups with different arsenic exposure levels. No statistical association was found between arsenic exposure and T2D. Our findings suggested that prolonged arsenic exposure might play a role in the development of hypertension; however, only high-level arsenic was associated with the risk of hypertension. Our findings also indicated that lower DMA% might be related with the increased susceptibility of arsenic-induced hypertension.

Effects of arsenite on glutamate metabolism in primary cultured astrocytes.

The aim of this study was to explore the mechanisms that contribute to neurotoxicity induced by arsenite exposure focusing on the alteration of glutamate metabolism in primary cultured astrocytes. The cells were exposed to 0-30µM arsenite for 24h, and then cell viability, intracellular nonprotein sulfhydryl (NPSH) levels, mitochondrial membrane potential, activity of Na(+)/K(+)-ATPase, glutamine synthetase (GS) and glutamate transporter (GLAST and GLT-1), and protein expression of GS, GLAST and GLT-1 were examined. Compared with those in control, exposure to arsenite resulted in damages of astrocytes in a concentration dependent manner, which were shown by cell viabilities, and supported by morphological observation, mitochondrial membrane potential and intracellular NPSH levels. On the other hand, activities and protein expression of GS, GLAST and GLT-1 were significantly inhibited by arsenite exposure. Moreover, protein expression of GLAST and activities of GS were much more sensitive to arsenite. However, activities of Na(+)/K(+)-ATPase were not influenced obviously by arsenite exposure. In conclusion, findings from this study indicated that exposure to arsenite could inhibit glutamate metabolism in astrocytes, which might be related to arsenic-induced neurotoxicity.

Effects of exogenous methionine on arsenic burden and NO metabolism in brain of mice exposed to arsenite through drinking water.

The aim of this study was to explore the effects of exogenous methionine (Met) on arsenic burden and metabolism of nitric oxide (NO) in the brain of mice exposed to arsenite via drinking water. Mice were exposed to sodium arsenite through drinking water contaminated with 50 mg/L arsenic for four consecutive weeks, and treated intraperitoneally with saline solution, 100 mg/kg body weight (b.w), 200 mg/kg b.w or 400 mg/kg b.w of Met, respectively at the fourth week. Levels of inorganic arsenic (iAs), monomethylarsenic acid (MMAs), and dimethylarsenic acid (DMAs) in the liver, blood and brain were determined by method of hydride generation coupled with atomic absorption spectrophotometry. Nitric oxide synthase (NOS) activities and NO levels in the brain were determined by colorimetric method. Compared with mice exposed to arsenite alone, administration of Met increased significantly the primary methylation ratio in the liver, which resulted in decrease of percent iAs and increase of percent DMAs in the liver, and decrease of iAs, MMAs and total arsenic levels (TAs) in the blood and DMAs and TAs in the brain. NOS activities and NO levels in the brain of mice exposed to arsenite alone were significantly lower than those in control, however administration of Met could increase significantly NO levels. Findings from this study suggested that exogenous Met could benefit the primary arsenic methylation in the liver, which might increase the production of methylated arsenicals and facilitate arsenic excretion. As a consequence, arsenic burden in both blood and brain was reduced, and toxic effects on NO metabolism in the brain were ameliorated.

[Influence of 1, 2-dichloroethane on open field behavior and levels of neurotransmitters in brain of mice].

OBJECTIVE: To explore the effects of 1,2-dichloroethane (1,2-DCE) on the behavior and the brain neurotransmitter levels in mice. METHODS: Thirty mice were randomly divided into four groups, which were control group and groups of low, middle and high exposure (225, 450 and 900 mg/m3) to 1,2-DCE for 10 days (3.5 h a day) by inhalation. After the last exposure, the open field test was performed immediately. After exposure all mice were killed and the brain tissues were taken up rapidly. The levels of aspartate (Asp), glutamate (Glu) and gamma-aminobutyric acid (GABA) in the brain were detected by high performance liquid chromatography (HPLC). RESULTS: Levels of Asp and Glu in all exposure groups increased with doses. As compared to the control group, levels of Glu in all exposure groups increased significantly (P < 0.05). Levels of GABA in the low exposure group were significantly lower than those in control group, but those in the high exposure group were significantly higher than those in control group. The results of the open field test showed that effect of low exposure to 1,2-DCE on the behavior was stimulant, but the high exposure to 1,2-DCE inhibited behavior of exploration, excitement and sport. CONCLUSIONS: Subacute exposure to 1,2-DCE could result in the change of amino acid neurotransmitter content and ratio in the brain, thereby change the behavior of mice appeared, which might be the mechanism of neurotoxicity caused by 1,2-DCE in part.

Effects of exogenous glutathione on arsenic burden and NO metabolism in brain of mice exposed to arsenite through drinking water.

Chronic exposure to inorganic arsenic (iAs) is associated with neurotoxicity. Studies to date have disclosed that methylation of ingested iAs is the main metabolic pathway, and it is a process relying on reduced glutathione (GSH). The aim of this study was to explore the effects of exogenous GSH on arsenic burden and metabolism of nitric oxide (NO) in the brain of mice exposed to arsenite via drinking water. Mice were exposed to sodium arsenite through drinking water contaminated with 50 mg/L arsenic for 4 weeks and treated intraperitoneally with saline solution, 200 mg/kg body weight (b.w), 400 mg/kg b.w, or 800 mg/kg b.w GSH, respectively, at the 4th week. Levels of iAs, monomethylarsenic acid, and dimethylarsenic acid (DMAs) in the liver, blood, and brain were determined by method of hydride generation coupled with atomic absorption spectrophotometry. Activities of nitric oxide synthase (NOS) and contents of NO in the brain were determined by colorimetric method. Compared with mice exposed to arsenite alone, administration of GSH increased dose-dependently the primary and secondary methylation ratio in the liver, which caused the decrease in percent iAs and increase in percent DMAs in the liver, as a consequence, resulted in significant decrease in iAs levels in the blood and total arsenic levels in both blood and brain. NOS activities and NO levels in the brain of mice in iAs group were significantly lower than those in control; however, administration of GSH could increase significantly activities of NOS and contents of NO. Findings from this study suggested that exogenous GSH could promote both primary and secondary arsenic methylation capacity in the liver, which might facilitate excretion of arsenicals, and consequently reduce arsenic burden in both blood and brain and furthermore ameliorate the effects of arsenicals on NO metabolism in the brain.

Distribution of speciated arsenicals in mice exposed to arsenite at the early life.

The aim of this study was to explore distribution of speciated arsenicals in mice exposed to arsenite at early developmental stages. Levels of speciated arsenicals in both liver and brain of mice were analyzed by hydride generation of volatile arsines, and determined by atomic absorption spectrophotometry (HG-AAS). In the liver, levels of inorganic arsenic (iAs) increased on postnatal day (PND) 15, and monomethylarsonic acid (MMA) increased on PND 21, however, levels of dimethylarsinic acid (DMA) in newborn mice were significantly higher than those on PND 10 and 15. In the brain, levels of iAs on PND 21 were the highest; iAs levels on PND 15 were also significantly higher than those on PND 35. Our results suggested transplacental transfer of arsenicals from pregnant mice into their fetus was relatively efficient, lactational transfer from mother mice into their offspring was inefficient, and transfer of iAs from blood into brain at early developmental stages was efficient.

Effects of exogenous GSH and methionine on methylation of inorganic arsenic in mice exposed to arsenite through drinking water.

We hypothesized that chronic exposure to arsenic would deplete the reduced glutathione (GSH) and methionine in vivo, thereby impair the methylation capacity of inorganic arsenic (iAs) ingested. Our experiment was designed to explore the effects of exogenous GSH and methionine on arsenic methylation in mice exposed to arsenite via drinking water. Levels of iAs, monomethylarsenic acid (MMAs), and dimethylarsenic acid (DMAs) in the liver and blood were determined by the method of hydride generation coupled with atomic absorption spectrophotometry. Compared with mice exposed to arsenite alone, administration of GSH or methionine increased the secondary methylation index in the liver and primary methylation index in the blood, which resulted in the consequent increase of DMAs percent and decrease of iAs percent in the blood. Moreover, administration of GSH resulted in the increase of DMAs percent in the liver and total arsenic in the blood. Increase of total arsenic in the blood was mainly due to the increase of DMAs. Findings from the present study suggested that administration of GSH or methionine might potentiate the methylation capacity of arsenic in both liver and extrahepatic tissues, which may facilitate the excretion of arsenic and decrease arsenic related toxicities in the body.

Distribution and speciation of arsenic by transplacental and early life exposure to inorganic arsenic in offspring rats.

The amount of arsenic compounds was determined in the liver and brain of pups and in breast milk in the pup's stomach in relation to the route of exposure: transplacental, breast milk, or drinking water. Forty-eight pregnant rats were randomly divided into four groups, each group was given free access to drinking water that contained 0, 10, 50, and 100 mg/L NaAsO(2) from gestation day 6 (GD 6) until postnatal day 42 (PND 42). Once pups were weaned, they started to drink the same arsenic-containing water as the dams. Contents of inorganic arsenic (iAs), monomethylarsonic acid (MMA), dimethylarsinic acid (DMA), and trimethylarsenic acid (TMA) in livers and brains of the pups on PND 0, 15, 28, and 42 and breast milk taken from the pup's stomach on PND 0 and 15 were detected using the hydride generation atomic absorption spectroscopy method. Concentrations of iAs, MMA, and DMA in the breast milk, the brain, and the liver of the pups increased with the concentration of arsenic in drinking water on PND 0, 15, 28, and 42. Compared to the liver or brain, breast milk had the lowest arsenic concentrations. There was a significant decrease in the levels of arsenic species on PND 15 compared to PND 0, 28, or 42. It was confirmed that arsenic species can pass through the placental barrier from dams to offspring and across the blood-brain barrier in the pups, and breast milk from dams exposed to arsenic in drinking water contains less arsenic than the liver and brain of pups.

Clinical manifestations and arsenic methylation after a rare subacute arsenic poisoning accident.

One hundred and four workers ingested excessive levels of arsenic in an accident caused by leakage of pipeline in a copper-smelting factory. Clinical examinations were performed by physicians in a local hospital. Excreted urinary arsenic species were determined by cold trap hydride generation atomic absorption spectrometry. In the initial toxic phase, gastrointestinal symptoms were predominant (83 people, 79.8%). Most patients showed leucopenia (72 people, 69.2%), and increased serum alanine aminotransferase (84 people, 80.8%) and aspartate aminotransferase (58 people, 55.8%). Thirty-five patients (33.6%) had elevated red blood cells in urine. After 17 days of admission, many subjects (45 people, 43.3%) developed peripheral neuropathy and 25 of these 45 patients (24.0%) showed a decrease in motor and sensory nerve conduction velocity. In the comparison of urinary arsenic metabolites among subacute arsenic-poisoned, chronic high arsenic-exposed and control subjects, we found that subacute arsenic-poisoned patients had significantly elevated proportions of urinary inorganic arsenic (iAs) and methylarsonic acid (MMA) but reduced proportion of urinary dimethylarsinic acid (DMA) compared with chronic high arsenic-exposed and control subjects. Chronic exposed subjects excreted higher proportions of iAs and MMA but lower proportions of DMA in urine compared with control subjects. These results suggest that gastrointestinal symptoms, leucopenia, and hepatic and urinary injury are predominant in the initial phase of subacute arsenic poisoning. Peripheral neuropathy is the most frequent manifestation after the initial phase. The biomethylation of arsenic decreases in a dose rate-dependent manner.