Mammals' immune systems react strongly to lipopolysaccharide, an endotoxin present in the outer membrane of gram -negative bacteria. Previous data show that the lipopolysaccharide challenge has a significant impact on reproductive function. This study aimed to explore the toxic effects of lipopolysaccharide on the uterine and ovarian tissues of female Wistar albino rats. Additionally, we investigated the effects of lipopolysaccharide on the expression of angiogenic and insulin growth factor 1 protein as well as oxidative stress markers in the uterus and ovaries. The experimental rats were allocated into two groups: (1) control group (n = 8): received intraperitoneal injection of pyrogen-free 0.9% NaCl and (2) treatment group (n = 12): single intraperitoneal injection of a non -lethal dose of lipopolysaccharide. Rats were sacrificed, and uterus and ovaries were collected at 6- and 72 -hour time points after lipopolysaccharide infusion. The exposure of the female rats to lipopolysaccharide induced a significant change in the antioxidant activity in both ovarian and uterine tissues especially after 72 hours of exposure. The exposure of nonpregnant rats to lipopolysaccharide leads to the degeneration of the ovarian follicles and superficial epithelium layer of the uterus. Also, the exposure of female rats to lipopolysaccharide leads to the upregulation of angiogenic proteins in both the ovaries and uterus and decreased expression of insulin growth factor 1 and insulin growth factor R1, especially after 72 hours. In conclusion, lipopolysaccharide is considered as one of the most potent bacterial virulence factors that causes endometrial inflammation and reproductive disorders.

Abstract Aims We investigated the effects of intraperitoneal injections of titanium dioxide nanoparticles (TiO2 NPs, 100 mg/kg) for 5 consecutive days on the developmental competence of murine oocytes. Furthermore, study the effects of TiO2 NPs on antioxidant and oxidative stress biomarkers, as well as their effects on expression of apoptotic and hypoxia inducing factor-1α (HIF1A) protein translation. Moreover, the possible ameliorating effects of intraperitoneal injections of fructose (2.75 mM/ml) was examined. Materials and methods Thirty sexually mature (8–12 weeks old; ~ 25 g body weight) female mice were used for the current study. The female mice were assigned randomly to three treatment groups: Group1 (G1) mice were injected intraperitoneal (ip) with deionized water for 5 consecutive days; Group 2 (G2) mice were injected ip with TiO2 NPs (100 mg/kg BW) for 5 consecutive days; Group 3 (G3) mice were injected ip with TiO2 NPs (100 mg/kg BW + fructose (2.75 mM) for 5 consecutive days. Results Nano-titanium significantly decreased expression of GSH, GPx, and NO, expression of MDA and TAC increased. The rates of MI, MII, GVBD and degenerated oocytes were significantly less for nano-titanium treated mice, but the rate of activated oocytes was significantly greater than those in control oocytes. TiO2 NPs significantly increased expression of apoptotic genes (BAX, Caspase 3 and P53) and HIF1A. Intraperitoneal injection of fructose (2.75 mM/kg) significantly alleviated the detrimental effects of TiO2 NPs. Transmission electron microscopy indicated that fructose mitigated adverse effects of TiO2 NPs to alter the cell surface of murine oocytes. Conclusion Results of this study suggest that the i/p infusion of fructose for consecutive 5 days enhances development of murine oocytes and decreases toxic effects of TiO2 NPs through positive effects on oxidative and antioxidant biomarkers in cumulus-oocyte complexes and effects to inhibit TiO2-induced increases in expression of apoptotic and hypoxia inducing factors.

This study was conducted to determine the polycyclic aromatic hydrocarbons (PAHs) levels and health risk of farm raw milk and ultra-heat treated (UHT) sterile market milk collected from different sources at Mansoura Province in Egypt using gas chromatography- mass spectrometry (GC- MS) during different seasons from August 2021 to December 2021. The results showed that the total amount of Σ18 PAHs levels was within the range of 11.778 – 26.331 µg/kg in farm milk samples and 1.151 – 2.946 µg/g in market UHT sterile milk. The results proved that the highest mean level of Σ PAHs in farm milk samples was 17.931 µg/kg followed by that of market sterile milk samples 2.123 µg/kg. European Commission (EC) has established safe level in milk for regulations require the concentrations of Benzo(a) pyrene (BaP) and the total Σ PAH4 to be less than 1.0 μg/kg. Mean concentration of BaP residues that was detected in farm milk samples was 0.251µg/kg with a range of 0.000 – 1.124 µg/kg and was not-detected in all market milk samples. Mean concentrations of Σ PAH4 levels were 0.561 µg/kg within the range of 0.046 – 2.433 µg/kg in farm milk and 0.047 µg/kg within the range of 0.012 – 0.110 µg/kg in market milk samples. These results were slightly higher than the critical limit set by the European Food Safety Authority (EFSA). The assessed dietary exposure was established by comparing the Estimated Daily Intake (EDI) with Acceptable Daily Intake (ADI). By comparing the obtained results, we found that for the BaP, the EDI for farm raw milk can be exceeded the maximum levels set in Regulation 1881/2006 (EFSA) for PAHs in milk, but UHT market sterile milk not exceeded the maximum levels. Therefore, there should be concerns regarding the effects of the consumption of different kinds of raw milk on the local population.

The potential reproductive toxic effects of oral TiO2 NPs in adult male rats as well as the possible alleviation of chitosan administration was investigated. Animals were allocated to four groups; the first group received deionized water and was assigned as a control group. In the second group, rats received chitosan at a dose of 5 mg/kg BW/day. The third group was designed for administration of TiO2 NPs at a dose of 150 mg/kg BW/day (1/80 LD50). Rats in the fourth group received both TiO2 NPs and chitosan. After 14 days, TiO2 NPs induced testicular lipid peroxidation as well as oxidative stress. Nano-titanium significantly upregulated genes that encode apoptosis and inflammation in testicular tissue. Moreover, it induced histological alteration in the testicular structure with impairment in spermatogenesis via reduction of PCNA immune-staining. Chitosan administration significantly improved the activities of testicular GPx, SOD, and CAT enzymes. In addition, it significantly down-regulated the relative expressions of pro-apoptotic and pro-inflammatory testicular genes. Chitosan was able to improve the testicular architecture as well as spermatogenesis. The current study revealed the capability of chitosan to ameliorate nano-titanium induced testicular toxicity. Thus, attention should be given to the extensive consumption of nano-titanium particles.

THE goal of the current study was to investigate the effects of fructose supplementation in the culture medium on in vitro maturation, and the developmental competence of murine oocytes, biochemical markers and the expression of apoptotic and HIF-1 alpha in cumulus oocyte cells (COCs). Murine oocytes were matured in IVF media supplemented with 1.25, 2.75 and 5-mM fructose. The developmental parameters (MI, MII, GVBD, degenerated and activated cells) were examined with NO, GPX, GSH, MDA, and TAC biomarkers. The expression of mRNA for apoptotic genes by COCs were evaluated. The low dosage improves significantly (P<0.05) the developmental competence markers than the control and higher doses of fructose. In vitro-matured mouse oocytes with 1.25 mM fructose showed a significant increase (P<0.05) in NO level in the In-vitro matured when compared with the control and other groups. The GPX concentrations in the in-vitro matured oocytes showed a significant decrease (P<0.05) with 5mM fructose. The MDA levels in the vitro-matured oocytes were higher (P<0.05) when the murine oocytes were exposed to 2.75 mM of fructose. The TAC in the oocyte showed no changes (P<0.05) when the oocytes were exposed to both 1.25 mM. Moreover, the supplementation of IVM media showed a down regulation of apoptotic and HIF-1 alpha genes when compared with the control and high dosage supplementation (P<0.05). Altogether, the supplementation of IVM media with lower dosage of fructose improves the developmental competence markers in the murine oocytes via its effects on oxidant and antioxidant activity and downregulation of apoptotic and HIF-1 alpha genes.

This study evaluated the structural changes, the immunohistochemical and gene expression of neurotrophic factors in submandibular gland in a rat model of depression, and their correlation with depression parameters during and after relief of depression by voluntary running. Forty-eight male Wistar rats were divided into control, control-exercise, depression, and depression-exercise groups. Depression was induced using forced swimming protocol, while the relief of depression was induced using the rat voluntary running wheels. The depressive state of rats was evaluated by measuring the immobility duration and the serum corticosterone level. The immune expression was evaluated by measuring the optical densities (ODs) using ImageJ software, and the gene expression levels were investigated. In the depression group, the convoluted ducts appeared dilated with numerous secretory granules. The number of PCNA-stained cells was significantly decreased in the depression group as compared to control group and then significantly increased in the depression-exercise group when compared to the depression group with a negative correlation to stress indicator. The ODs of immuno-expression for the brain-derived neurotrophic factor (BDNF) and vascular endothelial growth factor (VEGF) increased significantly in the depression group as compared to control group. Both BDNF and VEGF immuno-expression displayed positive correlation with the stress indicators. Both BDNF and VEGF gene expression results confirmed their immunohistochemical results. The findings of this study explored the role of submandibular gland in secreting neurotrophic factors and raise a flag for the possibility of using salivary secretions as dependable and easy parameter for estimation of chronic stressed patients.Mini AbstractThe submandibular gland neurotrophic factors immuno-expression can be used in estimating chronic depressive disorders as they are correlated with stress indicators during and after the relief of depression.

In the current study, we aimed to investigate the neurotoxic effect of oral titanium dioxide nanoparticles (TiO2 NPs) as well as the possible neuroprotective effect of carboxymethyl chitosan in adult rats for 14 days. The results revealed that TiO2 NPs inhibited the activity of the acetylcholine esterase enzyme and the levels of serotonin, dopamine, and norepinephrine neurotransmitters. Additionally, it induced neuro-oxidative stress and neuroinflammation via an elevation in MDA levels and IL-6, while GSH concentration, as well as GPx and GST activities, were decreased. TiO2 NPs induced neuronal apoptosis through upregulation of the expression of caspase-8 and -9 that was further confirmed by increasing caspases-3 and -8 proteins in the hippocampus, cerebral cortex, and cerebellum. The expression of the immediate-early gene BDNF was increased in response to TiO2 NPs, while that of Arc was reduced. Chitosan significantly attenuated the TiO2 NPs-induced neurotoxicity regarding AChE, serotonin, MDA, GSH, GPx, GST, IL-6, caspases-8, -9, and -3. Chitosan inhibited the expression of Arc and alleviated the effect of TiO2 NPs on BDNF expression. Collectively, TiO2 NPs induced neurotoxicity via their action on vital neuronal biomarkers that might in turn cause brain dysfunction. Despite the neuroprotection of chitosan, its inhibitory effect on Arc expression should be considered.

The human 15q13.3 microdeletion syndrome (DS) is caused by a heterozygous microdeletion (MD) affecting six genes: FAN1; MTMR10; TRPM1; KLF13; OTUD7A; and CHRNA7. Carriers are at risk for intellectual disability, epilepsy, autism spectrum disorder, and schizophrenia. Here we used the Df[h15q13]/+ mouse model with an orthologous deletion to further characterize molecular, neurophysiological, and behavioral parameters that are relevant to the 15q13.3 DS. First, we verified the expression and distribution of the α7 nicotinic acetylcholine receptor (nAChR), a gene product of the CHRNA7, in cortical and subcortical areas. Results revealed similar mRNA distribution pattern in wildtype (WT) and heterozygous (Het) mice, with about half the number of α7 nAChR binding sites in mutants. Hippocampal recordings showed similar input/output responses of field excitatory post-synaptic potentials and theta-burst induced long-term potentiation in WT and Het mice. Het males exhibited impaired spatial learning acquisition in the Barnes Maze. Indicative of increased seizure susceptibility, Het mice developed secondary seizures after 6-Hz corneal stimulation, and had significantly increased sensitivity to the chemoconvulsant pentylenetetrazol resulting in increased spiking in hippocampal EEG recordings. Basal mRNA expression of brain derived neurotrophic factor and activity regulated immediate early genes (c-fos, Arc, Erg-1 and Npas4) during adolescence, a critical period of brain maturation, was unaffected by genotype. Thus, the MD did not show gross neuroanatomical, molecular, and neurophysiological abnormalities despite deficits in spatial learning and increased susceptibility to seizures. Altogether, our results verify the phenotypic profile of the heterozygous Df[h15q13]/+ mouse model and underscore its translational relevance for human 15q13.3 DS.

The peri-implantation period of pregnancy is critical for conceptus development, implantation, and signaling for establishment of pregnancy. This study evaluated the effects of bisphenol A (BPA) on proliferation, adhesion, and migration of porcine trophectoderm (pTr2) cells, expression of transporters of arginine and synthesis of amino acids. All concentrations of BPA decreased proliferation and adhesion of pTr2 cells after 96 h compared to the control group. Lower concentrations of BPA (1 × 10−9, 1 × 10-8, 10-7M) increased (P < 0.05), but higher concentrations of BPA (1 × 10-5, 1 × 10-4 M) decreased migration of pTr2 cells. BPA increased expression of SLC7A1 mRNA at lower concentrations (1 × 10−9 to 1 × 10-6M) and SL7A6, another cationic acid transporter, at higher concentrations (1 × 10-5, 1 × 10-4 M). BPA also down-regulated the expression of IGF1 and IGF1 receptor at concentrations of 1 × 10-7 to 1 × 10-4 M compared to the control group. The expression of mRNAs for aquaporins (AQP) 3 and 4 were reduced at all concentrations of BPA, but at lower concentrations of BPA, (1 × 10−9 to 1 × 10-8M) expression of AQP9 mRNA increased and the expression of AQP11 was not affected by BPA (P > 0.05). There was an inhibitory effect of BPA on the release of synthesis of asparagine, threonine, taurine, tryptophan, and ornithine into the culture medium by pTr2 cells. Collectively, BPA adversely affected the expression of transporters for cationic amino acids like arginine, as well as AQPs, IGF1, and IGF1R associated with proliferation, migration, and adhesion of pTr2 cells. Those adverse effects would likely increase pregnancy losses during the peri-implantation period of pregnancy.

Objective: To evaluate the potential hazards of cadmium and/or chromium on the reproductive system of adult male albino rat. Design: Randomized controlled study. Animals: Forty mature male albino rats weighing 260 ± 10 g. Procedures: Rats were allocated into four groups (ten animals each). Control group (group 1), group 2 received 4.4 mg kg-1 cadmium chloride, group 3 was given 2.5 mg kg-1 sodium dichromate and group 4 received combination of Cd (2.2 mg kg-1) and Cr (1.25mg kg-1) orally, once daily for 65 consecutive days. Results: Exposure to Cd or Cr, in particular their combination, caused a reduction in the index weights of testes, epididymis, seminal vesicle and prostate glands. They induced a reduction of sperm count and viability with an increase of abnormal sperm morphology. Interestingly, in the combination group (Cd and Cr together), the deleterious effects were more noticeable. Pathologically, both Cd and Cr produced degenerative changes in seminiferous tubules, necrosis of spermatogenic epithelium within the testis. Moreover, the interstitial tissue of epididymis showed marked edema and prostate showed necrosis and serous exudate of lining epithelium. In the interaction group, testis showed complete degenerative changes and necrosis of spermatogenic epithelium, with marked interstitial edema and hyperplastic epithelial lining of epididymal tubules. Conclusion and clinical relevance: The present results support the hypothesis that the testis is one of the most sensitive organs to Cd and/or Cr and that the exposure to any of them or to their combination lead to testicular damage and thereby male infertility.

Carriers of the human 15q13.3 microdeletion (MD) present with a variable spectrum of neuropathological phenotypes that range from asymptomatic to severe clinical outcomes, suggesting an interplay of genetic and non-genetic factors. The most common 2MB 15q13.3 MD encompasses six genes (MTMR10, FAN1, TRPM1, KLF13, OTUD7A, and CHRNA7), which are expressed in neuronal and non-neuronal tissues. The nicotinic acetylcholine receptor (nAChR) alpha 7, encoded by CHRNA7, is a key player in the cholinergic anti-inflammatory pathway, and the transcription factor KLF13 is also involved in immune responses. Using a mouse model with a heterozygous deletion of the orthologous region of the human 15q13.3 (Df[h15q13]/+), the present study examined peripheral and central innate immune responses to an acute intraperitoneal (i.p.) injection of the bacteriomimetic, lipopolysaccharide (LPS) (100 mu g/kg) in adult heterozygous (Het) and wildtype (WT) mice. Serum levels of inflammatory markers were measured 2 h post injection using a Multiplex assay. In control saline injected animals, all measured cytokines were at or below detection limits, whereas LPS significantly increased serum levels of interleukin 1beta (IL-1 beta), tumor necrosis factor alpha (TNF-alpha), IL-6 and IL-10, but not interferony-gamma. There was no effect of genotype but a sexual dimorphic response for TNF-alpha, with females exhibiting greater LPS-induced TNF-alpha serum levels than males. In situ hybridization revealed similar increases in LPS-induced c-fos mRNA expression in the dorsal vagal complex in all groups. The hippocampal expression of the pro-inflammatory cytokines was evaluated by real-time quantitative PCR. LPS-treatment resulted in significantly increased mRNA expression for IL-1 beta, IL-6, and TNF-alpha compared to saline controls, with no effect of genotype, but a significant sex-effect was detected for IL-1 beta. The present study provided no evidence for interactive effects between the heterozygous 15q13.3 MD and a low-dose LPS immune challenge in innate peripheral or central immune responses, although, sex-differential effects in males and females were detected.

In forensic medicine, the study of gene expression in cadaveric tissues is well established, while analysis of post-mortem gene transcripts (thanatotranscriptome) is a novel arena for detection of post-mortem interval (PMI). In the current study, the brain tissues of three groups of rats (control (PMI = 0 h), room temperature (RT) and post-mortem heat-stress (HS-41 degrees C)) were examined for thanatotranscripts of particular genes using qRT-PCR at 1, 3 and 6 h post-mortem. In comparison with a control group, significant reductions were observed in the expression of genes-controlled apoptosis at all-time points, while expression of genes encode neuroinflammation recorded no obvious changes. C-fos showed expression under basal conditions. Post-mortem HS significantly induced the thanatotranscripts of testified genes at almost all time points. Positive correlation was reported between expression of IL-1 beta and Caspase-3 with PMI. Certain genes respond to post-mortem HS, which that accelerated the events that occurred in brain upon death, via induction of thanatotranscripts of genes that encode neuroinflammation, neuronal apoptosis and neuronal activation.

Bisphenol A (BPA) is an endocrinedisrupting chemical used in the manufacture of many products used daily. In the present study, the effects of BPA (1 x 10(-4) to 1 x 10(-9) M) on migration and on the expression of some apoptotic genes were examined in vitro using ovine trophectoderm (oTr1) primary cell line. The results revealed that BPA at 1 x 10(-9), 1 x 10(-8) and 1 x 10(-7)M increased migration of oTrl cells, while 1 x 10(-6), 1 x 10(-5) and 1 x 10(-4) M BPA decreased cell migration. Regarding apoptosis, expression of the anti-apoptotic gene Bcl-2 mRNA was greater at 1 x 10(-8) and 1 x 10(-9) M BPA and was downregulated at 1 x 10(-4) to 1 x 10(-7) M SPA; however, expression of pro-apoptotic genes (Bax, cathepsin B, caspase-3 and c-myc) was reduced at the higher concentrations of BPA. Results of this study suggest that SPA may impair implantation by decreasing migration of oTr1 cells and inhibiting apoptosis.

he present work was designed to investigate the reproductive toxicity induced by oral administration of chlorpyrifos (CPF), cypermethrin (CYP) and their combination in adult male albino rats. Forty mature male albino rats were separated into four groups (10 each), the first group was used as control, while second, third and fourth groups received orally 1/20 LD50 of CPF (10 mg/kg b.wt), 1/20 LD50 of CYP (17.22 mg/kg b.wt) and 1/40 LD50 of CPF plus 1/40 LD50 of CYP (5 mg/kg b.wt CPF plus 8.61 mg/kg b.wt CYP) respectively for 26 days. The results revealed that exposure to CPF and/or CYP induced a significant decrease in the reproductive organs weight. Moreover, a significant decrease in spermatic picture (sperm cell concentration and viability) was observed with high percent of sperm abnormalities. Serum levels of testosterone and pituitary gonadotropins (FSH and LH) have been declined significantly in all treated groups. Significant elevations were observed in malondialdehyde and nitric oxide concentrations, while antioxidant enzymes superoxide dismutase and glutathione-S-transferase activities were decreased significantly as a result of induced oxidative stress. A significant drop in prostatic acid phosphatase activity was observed. Additionally, the results showed some histopathological alterations in the reproductive organs as well as neurological lesions in brain and pituitary glands. In conclusion, CPF and CYP induce deleterious effects on reproductive efficiency of male rats which reflect more obvious impacts when both combined

Bisphenol A (BPA) is an endocrine disruptor with a weak estrogenic effect used in industry as a component of food cans. We aimed to study the toxic effects of BPA on mRNA expression of steroidogenic genes and testicular structure in mature male rats. Animals were divided into 3 groups: vehicle control rats as first group, while second group received 10 µg/kg BW and third group received BPA 15 µg/kg BW orally every alternate day for a period of 105 successive days. Serum testosterone level, mRNA expression of genes related to steroid synthesis, histopathological examination, spermatogenesis index and number of Leydig cells were evaluated in this study. Lower serum hormone levels were observed in both BPA-treated groups as compared to the control group. The gene expression patterns of steroidogenic acute regulatory protein (StAR), cytochrome P450 17a(CYP17a) and 3β-Hydroxysteroid dehydrogenase (3β-HSD) were significantly down-regulated in BPA-treated rats compared to control group. Meanwhile, the expression of aromatase (CYP19) and lutinizing hormone receptor (LHR) was significantly up-regulated. Histopathological lesions were observed in the testes and epididymis of BPA-treated rats. Spermatogenesis index and the number of Leydig cells were significantly decreased in BPA-treated groups compared with the control group. This study highlights negative effect of BPA on steroidogenic genes and testicular structure in male rats.

In the current study, The GC-MS metabolomics approach was used to evaluate the effect of cypermethrin on the metabolic profile in liver tissue of common carp fish. Fish were exposed to low and high concentrations of cypermethrin (0.1 and 1 µg/L respectively) for 24 and 96 h with subsequent PCA analysis to illustrate the response of the metabolic system after exposure to the pyrethroid. Cypermethrin induced obvious alteration in the intermediates of TCA cycle and encouraged consumption of non-carbohydrate sources in liver at all-time points. Additionally, cypermethrin exposure reduced the level of several amino acids and induced damage to the nucleotides reflecting the effect of cypermethrin on purine metabolism. GC-MS based metabolomics approach is a new and powerful tool to understand the toxicological effects and the underlying mechanism of cypermethrin on fish.

Maternal smoking has negative long-term consequences on affective behaviors, and in rodents, chronic neonatal nicotine exposure (CNN) results in increased anxiety. In rat pups, acute nicotine stimulation activates brain regions associated with stress and anxiety, but chronic nicotine exposure could desensitize of nicotinic acetylcholine receptors, the molecular target of nicotine. Here, we determined whether CNN affected neuronal activation by an acute nicotine challenge. Using in situ hybridization, we analyzed mRNA expression of the immediate-early genes (IEGs) c-Fos, Arc, Egr-1 and Npas4, which are markers for neuronal activation and implicated in synaptic plasticity. Following CNN (6 mg/kg/day) or control treatment from postnatal day (P)1 to P7, an acute i.p. nicotine (0.7 mg/kg) or saline injection (control) was administered on P8, and brains collected after 30 min. In drug-naive pups, acute nicotine stimulated IEGs expression specifically in brain areas associated with innate anxiety including the paraventricular hypothalamic nucleus, central nucleus of the amygdala (CeA), and locus coeruleus (LC). Following CNN, acute nicotine stimulated IEG expression in all three areas, but activation was significantly reduced in the LC (c-Fos, Egr-1, Npas4), and CeA (c-Fos). Notably, nicotine-induced Npas4 expression was greatly diminished in the LC, which may affect inhibitory synapse formation in noradrenergic neurons. Thus, after CNN, neurons located in areas associated with anxiety brain circuitry maintained responsiveness to nicotine, but tolerance differentially developed to nicotine. In the developing brain, repeated activation by nicotine of areas related to limbic pathways could alter circuit connectivity and increase responsiveness to stress and anxiety later in life. (C) 2018 Elsevier B.V. All rights reserved.

The present work designed to estimate postmortem expression of mRNA of certain hepatic genes in rats in the presence or absence of postmortem heat stress using qRT-PCR technique in correlation to postmortem interval (PMI). Rats were sacrificed and divided into, control group (PMI=0 h), room temperature and heat stressed (41⁰C) groups. In control group, liver samples were collected immediately after death, while in the second and third groups, samples were collected at 1, 3 and 6 hours postmortem. The results showed significant reductions in pro-inflammatory gene transcripts (TNFα and IL-1β) at all-time points compared to control group with an inhibitory effect of postmortem heat stress on expression of TNFα at 1 and 6 h after death. Whereas postmortem expression of genes encode apoptosis was significantly increased at 3 and 6 h postmortem compared to control group. Postmortem heat stress reduced the hepatic expression of Bcl-2 and Caspase-3 at 3 and 6 h of PMI and increased the expression of Caspase-3 at 1 h after death compared to room temperature group. Meanwhile, postmortem hepatic mRNA expression of c-fos was significantly induced after death at 3 and 6 h PMI. Postmortem heat stress significantly reduced c-fos expression at 3 and 6 h after death. Thanatotranscriptome of genes encode inflammation, apoptosis as well as c-fos varied in their correlations to PMI. Additionally, the results showed disparities in the effect of postmortem heat stress according to the studied gene and time.

Lipopolysaccharide (LPS) is a component of the outer membrane of gram negative bacteria. LPS challenging allows switching transcription of proinflammatory cytokines on via over stimulation of Toll-like receptors (TLRs) signaling pathway with subsequent pathogenic inflammatory response. We investigated the possible reproductive toxicity of LPS in male Wister albino rats. Oxidative stress markers, antioxidant status and caspase-3 activity were analyzed in testicular tissues of rats exposed to either saline or LPS (4 mg/kg BW, ip; 0.18 of the LD50). The samples were collected at 6 h and 72 h after injection of LPS. A significant reduction in testicular reduced glutathione (GSH), glutathione-S-transferase (GST) and superoxide dismutase (SOD) was observed at 72 h compared to control group. Total antioxidant capacity was decreased at 6 h with additional significant reduction at 72 h. Catalase activity was reduced significantly at both 6 and 72 h. Malondialdehyde (MDA) was increased (P ≤ 0.05) in LPS injected rats without variation between 6 and 72 h. A significant increase in nitric oxide (NO) was observed at 72 h after injection. A time-dependent increase in LPS-treated groups was observed in the concentration of caspase-3.Histopathological analysis revealed degenerative changes and necrosis of seminiferous tubules after 6 h with further accumulation of eosinophilic edematous transudate in its lumen after 72 h. In conclusion, by increasing time of exposure, LPS induced lipid peroxidation, oxidative stress, reduced testicular antioxidant capacity and encouraged testicular apoptosis which could be possible mechanisms for impairment of testicular function.