Exposure to Thiodan results in lipofuscin accumulation in hepatocytes of the freshwater catfish Tandanus tandanus

We investigated the effect of time after pulse exposure to 1.0 microg l(-1) endosulfan (applied as Thiodan) on endosulfan residues in the liver and ultrastructural changes in the hepatocytes of the freshwater catfish Tandanus tandanus. Time after exposure did not affect the mean residue level in the liver. After exposure to endosulfan, residues in the liver were 227.47 microg kg(-1) after 1 d and 282.83 microg kg(-1) after 28 d; residues in the bile were 313.97 microg kg(-1) after 1 d and 334.53 microg kg(-1) after 28 d. At the end of 28 d exposure, lipofuscin was present in up to 69% of hepatocytes of fish containing residues of endosulfan, but absent from control fish. There was a statistically significant increase in the percentage of pyknotic nuclei and altered rough endoplasmic reticulum 28 d after exposure. The mean percentage of cells with altered endoplasmic reticulum ranged from 12.93% (Day 1) to 7.50% (Day 28) for control fish, while for exposed fish it increased from 14.30% (Day 1) to 35.00% (Day 28). The mean percentage of cells with pyknotic nuclei increased from 1.1 to 2.1% in control fish and from 3.8 to 9.6% in exposed fish. Other ultrastructural changes included increased ultrastructural heterogeneity, progressive vacuolation and fractionation of rough endoplasmic reticulum, accumulation of lysosomes and residual bodies, intranuclear inclusions and pseudoinclusions, membrane whorls and myelinated bodies. Protracted senescence was one of the main features of endosulfan toxicity to T. tandanus hepatocytes.     

Impacts of fish oil on the gut microbiota of rats with alcoholic liver damage

The purpose of this study was to clarify the effects of fish oil on the gut microbiota of rats with alcoholic liver damage. Thirty-six male Wistar rats (8 weeks old) were divided into six groups: C (control), CF25 (control diet with 25% fish oil substitution), CF57 (control diet with 57% fish oil substitution), E (ethanol-containing diet), EF25 (ethanol-containing diet with 25% fish oil substitution), and EF57 (ethanol-containing diet with 57% fish oil substitution) groups. All groups were pair-fed an isoenergetic diet based on the E group. Rats were sacrificed after 8 weeks. Rats in the E group showed significant hepatic injuries including high plasma aspartate transaminase and alanine transaminase activities, hepatic cytokine levels, plasma endotoxin level, and protein expression of the toll-like receptor-4 signaling pathway; moreover, lipid accumulation and inflammation based on histological examinations were also observed. In contrast, these phenomena was ameliorated in rats of the EF25 and EF57 groups. Although the intestinal structure did not change among the groups, alterations in the gut microbiotic composition were observed due to chronic ethanol intake and fish oil replacement such as the Firmicutes-to-Bacteroidetes ratio, Chao-1 index, ACE index, a principal component analysis and linear discriminant analysis of effect size. In terms of the gut-liver axis, this study confirmed that fish oil replacement exerted ameliorative effects on ethanol-induced liver injuries in rats by acting through alterations in the microbiotic composition.     

Selenoprotein S is a marker but not a regulator of endoplasmic reticulum stress in intestinal epithelial cells

Selenoproteins are candidate mediators of selenium-dependent protection against tumorigenesis and inflammation in the gut. Expression and roles of only a limited number of intestinal selenoproteins have been described so far. Selenoprotein S (SelS) has been linked to various inflammatory diseases and is suggested to be involved in endoplasmic reticulum (ER) homeostasis regulation and antioxidative protection in a cell-type-dependent manner, but its protein expression, regulation, and function in the gut are not known. We here analyzed the expression and localization of SelS in the healthy and inflamed gut and studied its regulation and function in intestinal epithelial cell lines. SelS was expressed in the intestinal epithelium of the small and large intestine and colocalized with markers of Paneth cells and macrophages. It was upregulated in inflamed ileal tissue from Crohn's disease patients and in two models of experimental colitis in mice. We detected SelS in colorectal cell lines, where it colocalized with the ER marker calnexin. SelS protein expression was unaffected by enterocytic differentiation but increased in response to selenium supplementation and after treatment with the ER stress inducer tunicamycin. On the other hand, depletion of SelS in LS174T, HT29, and Caco-2 cells by RNA interference did not cause or modulate ER stress and had no effect on hydrogen peroxide-induced cell death. In summary, we introduce SelS as a novel marker of Paneth cells and intestinal ER stress. Although it is upregulated in Crohn's disease, its role in disease etiology remains to be established.     

昆虫肠道防御及微生物稳态维持机制

在长期的进化过程中,昆虫形成了独特的肠道防御系统,主要由物理屏障和免疫系统共同作用来抵御外来微生物的入侵。如大部分后生动物一样,昆虫肠道上皮细胞无时无刻不与微生物接触,其种类从有益的共生菌、随食物进入的微生物到影响宿主生命的病原菌。在这样一种复杂的环境中,为了实现防御肠道病原微生物的同时又能维持共生微生物稳定的目的,宿主肠道上皮细胞必须在免疫应激和免疫耐受之间保持一种稳态平衡。Duox-ROS免疫系统和免疫缺陷(immune deficiency,Imd)信号通路作为肠道免疫反应的基本途径,必然参与调节此过程。本文从昆虫肠道防御组成、肠道免疫信号通路作用分子机制以及肠道免疫系统在肠道微生物群落稳态维持中的作用的最新研究进展进行综述。     

Bioaccumulative potential and toxicity of endosulfan insecticide to non-target animals

1. Endosulfan insecticide is a polychlorinated compound used for controlling a variety of insects; it is practically water-insoluble, but readily adheres to clay particles and persists in soil and water for several years. Its mode of action involves repetitive nerve-discharges positively correlated to increase in temperature. This compound is extremely toxic to most fish and can cause massive mortalities. In fish, it causes marked changes in Na and K concentrations, decrease in blood Ca²⁺ and Mg levels and inhibits Na, K and Mg-dependent ATPase (in brain).2. Bioaccumulation of endosulfan is reported for marine animals; however, freshwater animals (e.g. crayfish) accumulate it to some extent, but they lose the compound rapidly during depuration. Endosulfan is generally less toxic to aquatic invertebrates than fish. However, it causes decreases in adenylate energy charge, oxygen consumption, hemolymph amino acids, succinate dehydrogenase, heart-beat (mussel) and altered osmoregulation.3. Generally, mammals are less susceptible to endosulfan's toxicity than aquatic animals. The majority of studies conducted on laboratory mammals can be summarized, (a) Neurotoxicity: male rats are more sensitive than females to endosulfan, which decreases brain and plasma acetyleholinesterase activity. Endosulfan I (a metabolite) causes a significant change in norepinephrine, 5-HT and GABA. (b) Renal toxicity: inhibition of MFOs activity was noticed in rats; other effects included changes in proximal convoluted tubules and necrosis of the tubular epithelium, (c) Hepatotoxicity: chemically-induced aminopyrine N-demethylase and aniline hydrolase were found in rat liver, and reduction in the glycogen level occurred, (d) Hematologic toxicity: endosulfan exposure resulted in a significant decrease in the erythrocyte glutathione reductase, hemoglobin amount, RBC number and mean corpuscular volume.4. Respiratory toxicity: involved dyspnea, acute emphysema, cyanosis and hemorrhages in the interalveolar partitions of rat's lungs.5. Biochemical: in rats, endosulfan caused increased glucose-6-phosphate dehydrogenase activity, blood glucose level, phospholipid contents of the microsomal and surfactant system, and profoundly induced the activity of alcohol dehydrogenase and cytosolic glutathione S-transferases. It also decreased significantly Na⁺, K⁺ and Mg²⁺ ATPases, plasma calcium level and alkaline phosphatase in the intestinal epithelium.6. Immunologic toxicity: rat serum antibody titer to tetanus toxin, IgG, IgM and gammaglobulins were significantly reduced.7. Reproductive toxicity: degenerative changes in the seminiferous epithelium, induction of the rate-limiting enzyme in testosterone production (3β-hydroxysteroid transferase and 17β-hydroxysteroid transferase), histological changes in reproductive organs, testicular atrophy and the occurrence of ovarian cysts were noticed in rat. Reduction in the weight of secondary sex organ was also observed.8. Developmental, teratogenic and genotoxicity: this insecticide caused a significant increase in the fetal résorption of rats. Skeletal abnormalities included underweight fetuses, small 4th and 5th unossified sternabrae. No fetotoxic or teratogenic activity was found in rabbits; however, in chickens, egg-hatchability and sterility occurred due to antimitotic activity. Endosulfan caused significant chromosomal aberrations in mouse and hamster bone-marrow cells and damage to spermatozoa cells. In Drosophila, sex-linked recessive lethals were noticed. In mice, dominant lethal mutations occurred; increase in abnormal sperm and decrease in count occurred.9. Carcinogenic toxicity: not reported to be carcinogenic in B6C3F mice or humans by any route of exposure.10. Toxicity to humans: endosulfan exposure has exhibited epileptic effects, hyperactivity, irritability, tremors, convulsions and paralysis in humans. A suicidal attempt by a 20-year old male who ingested 30% endosulfan caused hypoxia, followed by recurrent aspiration pneumonia, episodes of tachycardiogenic shock which was preceded by tachycardia and hypertension.     

The interplay between host cellular and gut microbial metabolism in NAFLD development and prevention

Metabolism regulation centred on insulin resistance is increasingly important in nonalcoholic fatty liver disease (NAFLD). This review focuses on the interactions between the host cellular and gut microbial metabolism during the development of NAFLD. The cellular metabolism of essential nutrients, such as glucose, lipids and amino acids, is reconstructed with inflammation, immune mechanisms and oxidative stress, and these alterations modify the intestinal, hepatic and systemic environments, and regulate the composition and activity of gut microbes. Microbial metabolites, such as short-chain fatty acids, secondary bile acids, protein fermentation products, choline and ethanol and bacterial toxicants, such as lipopolysaccharides, peptidoglycans and bacterial DNA, play vital roles in NAFLD. The microbe–metabolite relationship is crucial for the modulation of intestinal microbial composition and metabolic activity. The intestinal microbiota and their metabolites participate in epithelial cell metabolism via a series of cell receptors and signalling pathways and remodel the metabolism of various cells in the liver via the gut–liver axis. Microbial metabolic manipulation is a promising strategy for NAFLD prevention, but larger-sampled clinical trials are required for future application.     

猕猴发育过程中肠肝组织生长抑素及其受体表达演变规律

探讨在猕猴发育过程中生长抑素(somatostatin,SST)及其受体在肠肝组织的演变规律。通过手术途径获得胚胎6月、新生2 d、新生45 d和成年猕猴的回肠、肝脏、门静脉和外周血等标本。应用放射免疫分析法测定各标本中的SST含量; 通过免疫组化方法观察SST在肠、肝组织内的分布;利用原位杂交检测SST受体2(somatostatin receptor 2,SSTR2)的表达。结果显示:(1)胚胎6月的猕猴,小肠内SST含量为(27．3±16．6)ng／mg蛋白;黏膜隐窝处SST呈弱阳性染色,肌层 SST染色阴性。在发育过程中,小肠内SST含量逐渐增加,成年期时达最高水平(120．1±35．3)ng／mg蛋白,较胚胎6月显著增加(P<0．01)。(2)成年小肠黏膜隐窝处及肌间神经丛SST呈强阳性染色。(3)胚胎6月,小肠粘膜上皮可见大量SSTR2 表达,成年时SSTR2表达下调,且主要定位于腺上皮隐窝处;胚胎及新生期肌层SSTR2染色阴性,成年时小肠肌间神经丛则可见阳性SSTR2染色。(4)肝脏在发育过程中SST及SSTR2含量逐渐降低;发育的各个时期,小肠组织的SST含量均明显高于肝脏组织含量,门静脉SST水平也始终高于外周血。总之,位于小肠黏膜隐窝处的SST和SSTR2随着发育逐渐增加,来自肠道的SST进入门静脉后迅速被降解。SST阳性的肠肌间神经丛仅在发育成熟后才出现。     

Comparison of dietary and waterborne exposure to benzo a pyrene: bioavailability,tissue disposition and CYP1A1 induction in rainbow trout Oncorhynchus mykiss

Absorption and tissue distribution of benzo\[ a ]pyrene (BaP)-derived radioactivity were studied in juvenile rainbow trout following dietary or waterborne exposure. In order to compare the bioavailability of BaP, the fish were exposed to 1.5 mCi 3H-BaP kg-1 fish, either in the diet or in the water as a 2 days static exposure. Furthermore, tissue levels of BaP-derived radioactivity bound to macromolecules in different tissues were studied in non-induced fish, and in fish induced by additional treatment with unlabelled BaP (corresponding to 5 mg kg-1 fish) in the water. Absorption and tissue distribution of 3H BaP were studied by liquid scintillation counting and whole-body autoradiography. BaPderived radioactivity bound to macromolecules in different tissues was studied by autoradiography of solvent-extracted whole-body sections. The hepatic CYP1A induction was measured as EROD activity. Exposure to unlabelled BaP resulted in a marked induction of hepatic EROD activity in rainbow trout 2 days after the start of the exposure. Significant higher concentrations of radiolabelled compound were observed in waterborne-exposed fish, in contrast to dietary-exposed fish. High concentrations of radiolabelling were observed in the gills, liver, bile, intestines, olfactory organ, kidney and the skin of the waterborne-exposed fish. In the dietary-exposed fish, high levels of radioactivity were observed in the intestines and the bile, whereas lower concentrations were present in the liver. Only traces of radioactive compound were observed in the gills. In contrast to waterborne-exposed fish, no radioactivity was detected in the olfactory organ or skin. In autoradiograms of sections extracted with a series of polar and non-polar solvents, a large fraction of radioactivity was still present in the gills, olfactory organ, liver, kidney, skin and intestinal mucosa of the waterborne-exposed fish, indicating that reactive BaP intermediates formed by CYP1A-mediated metabolism were bound to macromolecules in these tissues.     

Tissue specific expression and developmental regulation of two genes coding for rat fatty acid binding proteins

We have examined the tissue distribution and developmental regulation of two low molecular weight cytosolic fatty acid binding proteins. Based on their initial site of isolation, they have been referred to as liver and intestinal fatty acid binding proteins (FABP). Cloned cDNAs were used to probe blots of RNAs extracted from a wide variety of adult rat tissues as well as small intestine and liver RNA obtained from fetal, suckling, and weaning animals. The highest concentrations of "liver" FABP mRNA were found in small intestine and liver. "Intestinal" FABP mRNA is most abundant in small bowel RNA while only trace amounts were encountered in liver. Both mRNAs were detectable in stomach, colon, pancreas, spleen, lung, heart, testes, adrenal, and brain RNA at 1-8% the concentrations observed in small intestine. Accumulation of both mRNAs in the small intestinal epithelium increases during development. The mRNAs are first detectable between the 19th and 21st day of gestation. They undergo a coordinated 3-4-fold increase in concentration within the first 24 h after birth. Thereafter, gut levels of intestinal FABP mRNA remain constant during the suckling period while liver FABP mRNA increases an additional 2-fold. Liver FABP mRNA levels are also induced in hepatocytes during the first postnatal day but subsequently do not change during the suckling and weaning phase, despite marked alterations in hepatic fatty acid metabolism. These observations support the concept that the major role of these proteins is to facilitate the entry of lipids into cells and/or their subsequent intracellular transport and compartmentalization. The data also raise questions about the identity of extragastrointestinal FABPs.     

Immunological importance of the second gut segment of carp. I. Uptake and processing of antigens by epithelial cells and macrophages

Uptake and transport of soluble (ferritin) and particulate ( Vibrio anguillarum ) antigen from intestinal lumen to mucosal macrophages was studied using immunocytochemical and electron-microscopical techniques. Both antigens were taken up by epithelial cells of the second gut segment, reached the supranuclear vacuoles and were finally transported to large intraepithelial macrophages. In contrast with particulate antigen, antigenic determinants of ferritin were demonstrated in the basal part of the epithelium and appeared to be released at the mucosal site.
After anal intubation many small macrophages penetrated the intestinal epithelium, took up antigen and after 24 h disappeared again from the intestinal mucosa. This feature was antigen independent and also occurred after anal PBS-intubation. The larger, less mobile macrophages stayed in the intestinal epithelium and finally exposed antigenic determinants (of both antigens) at their outer surface, suggesting an antigen-presenting function. Whether these large macrophages can induce a local or mucosal immune response and whether the smaller mobile macrophages are involved in a systemic response is discussed.     

Fine Structure of the Hepatic Sacculations of Glossobalanus minutus (Enteropneusta,Hemichordata)

Abstract The hepatic region of Glossobalanus minutus is characterized by deep foldings of the dorsal side of the gut epithelium which affect the neighbouring tissues and structures: coelomic spaces, musculature and epidermis. The following cell types of the gut epithelium are described: vacuolated cells, undifferentiated cells, two types of mucous cells and two types of granular secretory cells. The nature and function of the different cell types are discussed. Data on the general ciliation and subepithelial nerve plexus of the gut epithelium are also given, with special mention of a possible neuroendocrine secretion towards the subjacent blood spaces. A well-developed blood sinus (gut sinus) lies between the gut and the visceral peritoneum. The ultrastructural features of the gut epithelium and its close association with the blood sinus point to an absorptive function. The coelomic cavity is reduced to a narrow space limited by two peritoneal sheets (visceral and parietal) of myoepithelial nature. Amoebocyte-like cells (coelomocytes) occur free in the coelomic fluid, and muscular, unicellular bridges are attached to both peritoneal walls across the coelomic space. The dorsal epidermis follows the gut foldings and is formed by flat, overlapping cells. The present observations are compared with previous histological, histochemical and ultrastructural data.     

Endosulfan increases seric interleukin-2 like (IL-2L) factor and immunoglobulin M (IgM) of Nile tilapia (Oreochromis niloticus) challenged with Aeromona hydrophila

Endosulfan is a persistent organochlorine insecticide which is extremely toxic to fish. It is known to induce immunological alterations in juvenile Nile tilapia (Oreochromis niloticus) such as increases in phagocytic activity and reactive oxygen species production of spleen macrophages. The purpose of the present study was to demonstrate the effects of acute exposure to a sublethal concentration of endosulfan (7 ppb, 96 h) on parameters of the adaptive humoral immune response of the aforementioned aquatic organism. The effect of endosulfan on the capacity of immune cells to produce interleukin-2 like (IL-2L) factor and immunoglobulin M (IgM) in response to a challenge with ½ LD50 of the infectious bacteria Aeromonas hydrophila was evaluated.Experimental results indicate that short, sublethal, endosulfan exposure triggers a succession of events beginning with non-specific activation of macrophages followed by an exacerbated synthesis of the IL-2L factor by activated B cells. This leads to significantly increased secretion of IgM and could in turn facilitate autoantibody production and the development of autoimmune pathologies.     

Interactions with M cells and macrophages as key steps in the pathogenesis of enterohemorrhagic Escherichia coli infections

Enterohemorrhagic Escherichia coli (EHEC) are food-borne pathogens that can cause serious infections ranging from diarrhea to hemorrhagic colitis (HC) and hemolytic-uremic syndrome (HUS). Translocation of Shiga-toxins (Stx) from the gut lumen to underlying tissues is a decisive step in the development of the infection, but the mechanisms involved remain unclear. Many bacterial pathogens target the follicle-associated epithelium, which overlies Peyer's patches (PPs), cross the intestinal barrier through M cells and are captured by mucosal macrophages. Here, translocation across M cells, as well as survival and proliferation of EHEC strains within THP-1 macrophages were investigated using EHEC O157:H7 reference strains, isogenic mutants, and 15 EHEC strains isolated from HC/HUS patients. We showed for the first time that E. coli O157:H7 strains are able to interact in vivo with murine PPs, to translocate ex vivo through murine ileal mucosa with PPs and across an in vitro human M cell model. EHEC strains are also able to survive and to produce Stx in macrophages, which induce cell apoptosis and Stx release. In conclusion, our results suggest that the uptake of EHEC by M cells and underlying macrophages in the PP may be a critical step in Stx translocation and release in vivo. A new model for EHEC infection in humans is proposed that could help in a fuller understanding of EHEC-associated diseases.     

Influence of dietary iron deficiency on acute metal intoxication

The influence of dietary iron deficiency on acute nickel, lead or cadmium toxicity as reflected by the induction of hepatic, renal and intestinal metallothionein (MT), disposition of the metals, and alterations in hematological parameters was investigated in rats. The administration of cadmium induced the hepatic, renal and intestinal MT while that of nickel or lead induced hepatic MT only. However, dietary iron deficiency did not influence the cadmium induced tissue MT but enhanced the ability of nickel or lead to restore the normal synthesis of renal and intestinal MT lowered under the influence of reduced body iron status. The accumulation of lead in liver and kidney and that of cadmium enhanced in liver only, while tissue deposition of nickel remained unaffected by iron deficiency. The induction of hepatic MT by three metals appears related to the concomitant rise in the hepatic zinc, calcium and iron levels in normal rats. However, dietary iron deficiency increased the hepatic zinc in response to nickel or cadmium and that of heptic calcium in response to lead.     

Chemical chaperones reduce ionizing radiation-induced endoplasmic reticulum stress and cell death in IEC-6 cells

Radiotherapy, which is one of the most effective approaches to the treatment of various cancers, plays an important role in malignant cell eradication in the pelvic area and abdomen. However, it also generates some degree of intestinal injury. Apoptosis in the intestinal epithelium is the primary pathological factor that initiates radiation-induced intestinal injury, but the mechanism by which ionizing radiation (IR) induces apoptosis in the intestinal epithelium is not clearly understood. Recently, IR has been shown to induce endoplasmic reticulum (ER) stress, thereby activating the unfolded protein response (UPR) signaling pathway in intestinal epithelial cells. However, the consequences of the IR-induced activation of the UPR signaling pathway on radiosensitivity in intestinal epithelial cells remain to be determined. In this study, we investigated the role of ER stress responses in IR-induced intestinal epithelial cell death. We show that chemical ER stress inducers, such as tunicamycin or thapsigargin, enhanced IR-induced caspase 3 activation and DNA fragmentation in intestinal epithelial cells. Knockdown of Xbp1 or Atf6 with small interfering RNA inhibited IR-induced caspase 3 activation. Treatment with chemical chaperones prevented ER stress and subsequent apoptosis in IR-exposed intestinal epithelial cells. Our results suggest a pro-apoptotic role of ER stress in IR-exposed intestinal epithelial cells. Furthermore, inhibiting ER stress may be an effective strategy to prevent IR-induced intestinal injury.     

Influence of larval feeding history on the body condition of Amphiprion melanopus

The cellular condition of liver hepatocytes and the height of gut epithelium cells of larval Amphiprion melanopus were sensitive indicators of feeding condition. Muscle fibres of the trunk showed marked separation in fish fed every third day just prior to settlement. Low feeding regimes also caused reductions in growth, increases in larval duration and reductions in size at metamorphosis. Gut epithelium cell height was also influenced by fish standard length and age. This study suggests that gut epithelium cell height is a useful index for an examination of the importance of starvation of larvae in tropical waters; however, size and age standardization is required prior to comparisons of wild caught fish through time or with laboratory samples.     

Gut peptide and neuroendocrine regulation of hepatic lipid and lipoprotein metabolism in health and disease

Non-alcoholic fatty liver disease (NAFLD) is a continuum of disorders that can range from simple steatosis to non-alcoholic steatohepatitis (NASH). As a complex metabolic disorder, the pathophysiology of NAFLD is incompletely understood. Recently glucagon-like peptide (GLP)-1 and -2 signalling has been implicated in the pathogenesis of NAFLD. The role of these gut hormones in the hepatic abnormalities is complicated by lack of consensus on the presence of GLP-1 and GLP-2 receptors within the liver. Nevertheless, GLP-1 and GLP-2 receptor agonists have been associated with alterations in lipid metabolism and hepatic and systemic inflammation, pathological abnormalities characteristic of NAFLD. Treatment with GLP-1 analogues has been shown to reverse features of NAFLD including insulin resistance, and alterations in hepatic de novo lipogenesis and reactive oxygen species. In this review, we provide an overview of the role of GLP-1 and GLP-2 in lipid homeostasis and metabolic disease including NAFLD and NASH.     

沙漠干热环境下猪腹部肠管火器伤后肝脏功能和形态的变化

目的:观察沙漠干热环境下猪腹部火器伤肠管穿透后肝脏功能和形态的变化。方法:沙漠干热环境组和常温环境组各健康长白仔猪42头随机等分为对照组和伤后1h、2h、4h、8h、12h和24h组,实验组建立腹部火器伤肠管穿透模型后,分别测定各组动物血清中AST水平,并与对照组比较。在光镜下观察各组肝脏组织学变化,电镜下观察肝脏超微结构改变。结果:伤后各组血清AST水平均高于对照组,并于伤后2h出现第1个高峰,沙漠干热环境组和常温环境组分别于伤后8h和12h出现第2个高峰。沙漠干热组和常温组分别于伤后4h和8h开始出现肝细胞的坏死和超微结构的明显变化。结论:沙漠干热环境下腹部肠管火器伤后肝脏结构和功能损伤的发生均较常温组提前,提示在沙漠干热环境下腹部火器伤更要及早对肝损伤采取相应的保护措施。