Investigation of the effects of mechanical and underfloor heating systems on the COVID-19 viruses distribution.

Investigation of the spread of pollutants and especially pathogenic particles in the interior of today's buildings has become an integral part of the design of such buildings. When the Coronavirus is prevalent in the world, it is necessary to pay attention to the spread of the virus in the interior of residential apartments. In the present study, the Coronavirus particles emitted from the sneezing of a sick person in the bedroom of a residential apartment were tracked. Meanwhile, the degree of exposure of a mannequin that has been placed in the living room playing the role of a healthy person is examined. In this research, a segregated solution of steady-state flow and an unsteady particle solution have been separately used: a suitable, accurate, and optimal solution in particle studies. A comparison of the results shows that underfloor heating creates a healthier space around the healthy person's respiratory system, but instead, we will see more polluted areas around the sick person. According to the PRE results, the PRE value for a mechanical heating system is higher than a floor heating system. Therefore, it is recommended to use mechanical heating system in the apartments where the person with COVID-19 is hospitalized.

Hormesis Effects of Nano- and Micro-sized Copper Oxide.

The concerns about the possible risk of manufactured nanoparticles (NPs) have been raised recently. Nano- and micro-sized copper oxide (CO and CONP) are widely used in many industries. In this regard, in-vitro studies have demonstrated that CONP is a toxic compound in different cell lines. Despite their unique properties, NPs possess unexpected toxicity profiling relative to the bulk materials. This study was designed to examine and compare the toxic effects of CO and CONPs in-vivo and in isolated rat mitochondria. Male Wistar albino rats received 50 to 1000 mg/kg CO or CONP by gavage and several toxicological endpoints including biochemical indices and oxidative stress markers. Then, the pathological parameters in the multiple organs such as liver, brain, spleen, kidney, and intestine were assessed. Mitochondria were isolated from the rat liver and several mitochondrial indices were measured. The results of this study demonstrated that CO and CONP exhibited biphasic dose-response effects. CONPs showed higher toxicity compared with the bulk material. There were no significant changes in the results of CONP and CO in isolated rat liver mitochondria. The present studies provided more information regarding the hormetic effects of CO and CONPs in-vivo and in isolated rat mitochondria.

Sulfasalazine induces mitochondrial dysfunction and renal injury.

Sulfasalazine is a commonly used drug for the treatment of rheumatoid arthritis and inflammatory bowel disease. There are several cases of renal injury encompass sulfasalazine administration in humans. The mechanism of sulfasalazine adverse effects toward kidneys is obscure. Oxidative stress and its consequences seem to play a role in the sulfasalazine-induced renal injury. The current investigation was designed to investigate the effect of sulfasalazine on kidney mitochondria. Rats received sulfasalazine (400 and 600 mg/kg/day, oral) for 14 consecutive days. Afterward, kidney mitochondria were isolated and assessed. Sulfasalazine-induced renal injury was biochemically evident by the increase in serum blood urea nitrogen (BUN), gamma-glutamyl transferase (γ-GT), and creatinine (Cr). Histopathological presentations of the kidney in sulfasalazine-treated animals revealed by interstitial inflammation, tubular atrophy, and tissue necrosis. Markers of oxidative stress including an increase in reactive oxygen species (ROS) and lipid peroxidation (LPO), a defect in tissue antioxidant capacity, and glutathione (GSH) depletion were also detected in the kidney of sulfasalazine-treated groups. Decreased mitochondrial succinate dehydrogenase activity (SDA), mitochondrial depolarization, mitochondrial GSH depletion, increase in mitochondrial ROS, LPO, and mitochondrial swelling were also evident in sulfasalazine-treated groups. Current data suggested that oxidative stress and mitochondrial injury might be involved in the mechanism of sulfasalazine-induced renal injury.

Carnosine ameliorates liver fibrosis and hyperammonemia in cirrhotic rats.

AIM: Chronic liver injury and cirrhosis leads to liver failure. Hyperammonemia is a deleterious consequence of liver failure. On the other hand, oxidative stress seems to play a pivotal role in the pathogenesis of liver fibrosis as well as in the cytotoxic mechanism of ammonia. There is no promising therapeutic agent against ammonia-induced complications. The present study was conducted to evaluate the role of carnosine (CA) administration on liver pathological changes, elevated plasma ammonia, and its consequent events in cirrhotic rats. METHODS: Bile duct ligated (BDL) rats were used as a model of cirrhosis. CA (250, 500, and 1000mg/kg, daily, i.p) was administered for 28 consecutive days to BDL animals. At the end of treatments, markers of oxidative stress and liver fibrosis was determined in liver and serum biomarkers of liver injury and plasma ammonia was assessed. Moreover, changes in animals' locomotor activity were monitored. RESULTS: Severe bridging fibrosis, inflammation, and necrosis in liver, along with elevated serum biomarkers of liver injury were evident in BDL animals. Furthermore, plasma ammonia was drastically elevated in cirrhotic rats and animals' locomotor activity was suppressed. It was found that CA (250, 500, and 1000mg/kg, daily, i.p) significantly alleviated liver injury and its consequent events in cirrhotic rats. The data suggested that CA is not only a useful and safe agent to preserve liver function, but also prevented hyperammonemia and brain damage as a deleterious consequence of cirrhosis and liver failure.

Disturbance of zinc and glucose homeostasis by methyl tert-butyl ether (MTBE); evidence for type 2 diabetes.

1. The prevalence of diabetes and the other metabolic disorders has noticeably increased worldwide. A causal link between increasing risk of type 2 diabetes and exposure to environmental pollutants has been reported. 2. We hypothesized that exposure to methyl tert-butyl ether (MTBE), an oxygenate additive to gasoline would hinder zinc and glucose homeostasis in rats. 3. Male Sprague-Dawley rats received MTBE in drinking water for 90 days. At the end of the treatment, pancreas and blood samples were collected for biochemical and molecular examinations. Expression of four candidate genes, including Insulin1, Insulin2, MT1A, SLC30A8 by Real-Time Quantitative PCR (Q-PCR) as well as biochemical parameters, including fasting blood glucose (FBS), triglycerides (TG), cholesterol (CHO), low-density lipoprotein (LDL), high-density lipoprotein (HDL), copper (Cu2+) and calcium (Ca2+) levels as well as High-sensitive C-reactive protein were assessed as endpoints. 4. This study suggested that MTBE exposure can be associated with disruption in zinc homeostasis and glucose tolerance.

Exposure to methyl tert-butyl ether (MTBE) is associated with mitochondrial dysfunction in rat.

1. Methyl tert-butyl ether (MTBE) is commonly used as an octane booster and oxygenate additive to gasoline. The assumed toxic effects of MTBE on human health are a matter of great debate. Exposure to MTBE has been shown to induce oxidative damage and no mechanistic explanation is available so far. Our goals were to determine whether MTBE is a mitochondrial toxicant, if so, what mechanism(s) is involved. 2. Male Sprague-Dawley rats were received MTBE in drinking water for 3 months. At the end of treatments, animals were killed, liver and blood samples were collected for biochemical and histopathological studies, and oxidative stress biomarkers. The rat liver mitochondria were isolated and several mitochondrial indices were measured. 3. We found that zinc plasma levels were remarkably declined with MTBE and N, N, N', N'-Tetrakis (2-pyridylmethyl) ethylenediamine (TPEN; a zinc chelator) exposure. MTBE induced oxidative damage and caused mitochondrial dysfunctions in rats. Supplementation with zinc was able to protect against MTBE-induced cellular and sub-cellular toxicity. 4. Our results demonstrated that long-term exposure to MTBE is associated with zinc deficiency, oxidative stress, and mitochondrial energy failure in rat.

Metabolic and endocrine effects of bisphenol A exposure in market seller women with polycystic ovary syndrome.

Bisphenol A (BPA) is one of the synthetic monomer which can be found in the environment. Limited animal and human studies have demonstrated that BPA alters endocrine and or metabolic functions. The aims of the present study were to evaluate serum BPA level in marketing seller women with polycystic ovary syndrome (PCOS) and hormonal and metabolic effects of this exposure compared to a control paired group. In a case-control study, 62 PCOS women who work as marketing sellers and 62 healthy women with similar jobs were included. The two groups were body mass index (BMI)- and age-matched. Serum samples were analyzed for BPA content, fasting blood sugar (FBS), triglyceride, cholesterol, HDL and LDL levels, thyroid stimulating hormone (TSH) concentration, and LH:FSH ratio. Significant higher serum BPA content (0.48 ± 0.08 vs. 0.16 ± 0.04 ng/ml), triglyceride (103.05 ± 13.10 vs. 91.65 ± 12.52 mg/dl), cholesterol (165.05 ± 10.79 vs. 161.21 ± 10.31 mg/dl) levels and LH:FSH ratio (3.64 ± 0.86 vs. 0.62 ± 0.14) and significant lower TSH concentration (1.56 ± 0.68 vs. 2.15 ± 1.09 IU/ml) were detected in case against control group, respectively (P < 0.05). No significant differences were detected in FBS, LDL, and HDL levels between the two groups. Also, there were no significant associations between serum TSH concentration and BPA level neither in case (P = 0.269) nor in control (P = 0.532) groups. In BPA-exposed PCOS women, BPA level was higher than healthy women and this difference maybe the cause of significant differences in levels of triglyceride, cholesterol, TSH, and LH:FSH ratio. These observations confirm the potential role of BPA in PCOS pathophysiology.

Sulfasalazine-induced renal and hepatic injury in rats and the protective role of taurine.

INTRODUCTION: Sulfasalazine is a drug commonly administrated against inflammatory-based disorders. On the other hand, kidney and liver injury are serious adverse events accompanied by sulfasalazine administration. No specific therapeutic option is available against this complication. The current investigation was designed to evaluate the potential protective effects of taurine against sulfasalazine-induced kidney and liver injury in rats. METHODS: Male Sprague-Dawley rats were administered with sulfasalazine (600 mg/kg, oral) for 14 consecutive days. Animals received different doses of taurine (250, 500 and 1000 mg/ kg, i.p.) every day. Markers of organ injury were evaluated on day 15(th), 24 h after the last dose of sulfasalazine. RESULTS: Sulfasalazine caused renal and hepatic injury as judged by an increase in serum level of creatinine (Cr), alanine aminotransferase (ALT), aspartate aminotransferase (AST), lactate dehydrogenase (LDH), and alkaline phosphatase (ALP). The levels of reactive oxygen species (ROS) and lipid peroxidation were raised in kidney and liver of sulfasalazine-treated animals. Moreover, tissue glutathione reservoirs were depleted after sulfasalazine administration. Histopathological changes of kidney and liver also endorsed organ injury. Taurine administration (250, 500 and 1000 mg/kg/day, i.p) alleviated sulfasalazine-induced renal and hepatic damage. CONCLUSION: Taurine administration could serve as a potential protective agent with therapeutic capabilities against sulfasalazine adverse effects.

Concurrent Inflammation Augments Antimalarial Drugs-Induced Liver Injury in Rats.

Purpose: Accumulating evidence suggests that drug exposure during a modest inflammation induced by bacterial lipopolysaccharide (LPS) might increase the risk of drug-induced liver injury. The current investigation was designed to test if antimalarial drugs hepatotoxicity is augmented in LPS­treated animals. Methods: Rats were pre-treated with LPS (100 µg/kg, i.p). Afterward, non-hepatotoxic doses of amodiaquine (25, 50 and 100 mg/kg, oral) and chloroquine (25, 50 and 100 mg/kg, oral) were administered. Results: Interestingly, liver injury was evident only in animals treated with both drug and LPS as estimated by pathological changes in serum biochemistry (ALT, AST, LDH, and TNF-α), and liver tissue (severe hepatitis, endotheliitis, and sinusoidal congestion). An increase in liver myeloperoxidase enzyme activity, lipid peroxidation, and protein carbonylation, along with tissue glutathione depletion were also detected in LPS and drug co-treated animals. Conclusion: Antimalarial drugs rendered hepatotoxic in animals undergoing a modest inflammation. These results indicate a synergistic liver injury from co-exposure to antimalarial drugs and inflammation.

Effect of taurine on chronic and acute liver injury: Focus on blood and brain ammonia.

Hyperammonemia is associated with chronic and acute liver injury. There is no promising therapeutic agent against ammonia-induced complications. Hence, finding therapeutic molecules with safe profile of administration has clinical value. The present study was conducted to evaluate the role of taurine (TA) administration on plasma and brain ammonia and its consequent events in different models of chronic and acute liver injury and hyperammonemia. Bile duct ligated (BDL) rats were used as a model of chronic liver injury. Thioacetamide and acetaminophen-induced acute liver failure were used as acute liver injury models. A high level of ammonia was detected in blood and brain of experimental groups. An increase in brain ammonia level coincided with a decreased total locomotor activity of animals and significant changes in the biochemistry of blood and also liver tissue. TA administration (500 and 1000 mg/kg, i.p), effectively alleviated liver injury and its consequent events including rise in plasma and brain ammonia and brain edema. The data suggested that TA is not only a useful and safe agent to preserve liver function, but also prevented hyperammonemia as a deleterious consequence of acute and chronic liver injury.

Coenzyme Q10 remarkably improves the bio-energetic function of rat liver mitochondria treated with statins.

CoQ10 shares a biosynthetic pathway with cholesterol therefore it can be a potential target of the widely available lipid-lowering agents such as statins. Statins are the most widely prescribed cholesterol-lowering drugs with the ability to inhibit HMG-CoA (3-hydroxy-3-methylglutaryl-coenzyme A) reductase. Preclinical and clinical safety data have shown that statins do not cause serious adverse effects in humans. However, their long-term administration is associated with a variety of myopatic complaints. The aim of this study was to investigate whether CoQ10 supplementation of animals under high fat diet (HFD) treated with statins is able to bypass the mitochondrial metabolic defects or not? Animals were divided into 7 groups and fed with either regular (RD) or HFD during experiments. The first group considered as regular control and fed with a RD. Groups 2-7 including HFD control, CoQ10 (10mg/kg), simvastatin (30mg/kg), atorvastatin (30mg/kg), simvastatin+CoQ10 or atorvastatin+CoQ10 treated orally for 30 days and fed with HFD. At the end of treatments, the animals were killed and blood samples were collected for biochemical examinations. The rat liver mitochondria were isolated and several mitochondrial indices including succinate dehydrogenase activity (SDA), ATP levels, mitochondrial membrane potential (MMP) and mitochondrial permeability transition pore (MPP) were determined. We found that triglyceride (Tg), cholesterol (Chol) and low-density lipoprotein (LDL) were augmented with HFD compared to RD and treatment with statins remarkably lowered the Tg, Chol and LDL levels. Mitochondrial parameters including, SDA, ATP levels, MMP and MPP were reduced with statin treatment and improved by co-administration with CoQ10.

Hepatoprotective effect of silyamarin in individuals chronically exposed to hydrogen sulfide; modulating influence of TNF-α cytokine genetic polymorphism.

BACKGROUND AND THE PURPOSE OF THE STUDY: Silymarin, a standardized extract of the milk thistle (Silybum marianum), is believed to exert some of its hepatoprotective effects though inhibition of free radicals and inflammation. In this study the effect of some pro- and anti-inflammatory cytokines and also antioxidant genes polymorphisms on the hepatoprotective effects of silymarin in the occupationally exposed individuals to hydrogen sulfide (H2S) in the sour natural gas refinery was investigated. METHODS: We genotyped seven polymorphisms in six genes reported by others as modifiers of oxidative stress (NQO1, mEPXH1, GSTT1 and GSTM1) and inflammation (TNF-α and TGF-ß1) for an association in effect of decreasing in liver function tests (LFTs). The LFTs of 77 sour gas refinery workers were measured before and after administration of silymarin (140 mg, three times per day for 1 month). RESULTS: A significant reduction of blood AST, ALT and ALP was observed after 30 days of consumption (p < 0.001). The decreasing effect of silymarin on ALT in the subjects with high producer genotype (A allele carriers) was less than low producers. There were no significant associations between TGF-ß1 and the studied genes of oxidative stress pathway and the effectiveness of silymarin. CONCLUSION: This is the first report about the effectiveness of silymarin in the subjects exposed chronically to H2S. Meanwhile, the modulatory effect of TNF-α on the effectiveness of silymarin might be used for individualize therapy.