Congestion Of Central Vein Research Articles

Selenium-enriched yeast regulates aquaporins to alleviate atrazine-induced hepatic ionic homeostasis disturbance in Japanese quails

Atrazine (ATR), a commonly used herbicide, carries a risk to the health of humans and animals due to its persistence in the environment and accumulation in the body. The main metabolic processes of ATR was occurred in the liver. Therefore, the accumulation of ATR in the body can cause serious hepatic injury. This research aimed to clarify the toxicological effect of ATR and explore the potential protective benefits of selenium-enriched yeast (Yeast-Se) in alleviating liver toxicity induced by ATR. Quails were treated with ATR and Yeast-Se for 28 days. The results indicated that ATR inhibited quail growth and development and caused liver dysfunction. Pathological analysis showed that ATR led to central vein congestion and gallbladder epithelial cells shedding and necrosis. In addition, ATR significantly changed hepatic ion content (Na+, K+, Cl−, Ca2+, Mg2+) and decreased Na+-K+-ATPase and Ca2+/Mg2+-ATPase activities. Notably, supplementary Yeast-Se protects against ATR-induced liver ionic disorder by reversing ATPase activity and increasing ATPase subunits expression. In addition, supplementary Yeast-Se significantly up-regulated the expression of aquaporins (AQPs). In summary, these results indicated that Yeast-Se may regulates AQPs to alleviate ATR-induced ionic homeostasis disturbance in liver.

Exposure to tobacco (Nicotiana tabacum) extract and cigarette smoke induces hematological and histopathological alterations in Swiss albino mice

Tobacco smoking is a widely practiced recreational activity and is associated with numerous health risks. Hence, the present study was conducted on Swiss albino mice to assess the impact of aqueous extract of tobacco and cigarette smoke on behavioral, hematological, and histopathological parameters of the lungs, liver, and kidney. The mice were divided into Control (Cont), Tobacco nicotiana (TN), and Cigarette smoke (CS) groups (n=6). TN group received aqueous tobacco orally at a dose of 5ml/kg BW for 21 days, whereas CS group was exposed to inhalational commercial cigarette smoke for the same duration. On day 22, blood samples and visceral organs were collected to evaluate hematological (TEC, TLC, Hb%) and histopathological parameters from euthanized mice. The TEC values were significantly elevated (P<0.05) in both groups. In contrast to the control group, the TLC value was lower in the CS group (P>0.05) than in the TN group, but the mean Hb% values showed no significant changes. Lower body weight, aggressive behavior, and weakness were observed in the treated groups. Histopathologically, the lung revealed emphysematous changes, alveolar septal thickening, inflammatory cells infiltration, congestion, and thrombus formation in pulmonary artery. Liver exhibited hepatocyte degeneration with karyomegaly and karyorrhexis, derangement of hepatic cords and sinusoids with central vein congestion. Derangement of renal tubules, edema, and glomerular degeneration observed in the kidney. These observations lead us to postulate that tobacco and cigarette smoke exert detrimental effects on the structure of some vital organs in the body after direct or indirect uptake.

Hepatoprotective Effect of Alcoholic Extract of Ficus carica Leaves ‎Against ‎‎Cypermethrin-Induced Liver Toxicity in Male Albino Rats

Cypermethrin (CYP), a synthetic pyrethroid, is recognized for its insecticidal properties but ‎poses potential risks of hepatotoxicity. In traditional medicine, Ficus (F.) carica (common ‎fig) leaves have historically been used for various therapeutic applications. This study ‎aimed to evaluate the hepatoprotective effect of the methanolic extract of F. carica‎‎ leaves ‎against CYP-induced liver damage in adult male albino rats (Rattus norvegicus). The ‎animals (n=30), 8-12 weeks old ‎and weighing 200-250 g‎, were randomly divided into five ‎experimental groups (n=6) and treated as follows: the negative control group received ‎distilled water; the CYP-Only group was exposed to 4.74 mg/kg BW for 45 days; the ‎CYP+post-treatment group received the same CYP dosage followed by F. carica‎‎ methanolic ‎leaf extract at 500 mg/kg BW orally for two weeks; the pre-treatment+CYP group received ‎ ‎F. carica‎‎ methanolic leaf extract at 500 mg/kg BW orally for two weeks followed by CYP ‎exposure for 45 days; and the F. carica‎‎ extract-Only group was administered the methanolic ‎leaf extract at 500 mg/kg BW orally for two weeks. At the end of the experiment, serum and ‎liver samples were analyzed for biochemical and histopathological changes. CYP-Only ‎exposed group showed significantly increased serum alanine aminotransferase (ALT) and ‎alkaline phosphatase (ALP) and caspase-3 levels (P<0.05). Histopathological examination ‎in group exposed CYP only revealed liver damages as evidenced by central vein congestion, ‎scattered perivascular mononuclear cell infiltration, prominence of ‎Kupffer cells, nuclear ‎pyknosis, and severe hepatocytic necrosis. Treatment with F. carica‎‎ leaf extract, either ‎before or after CYP exposure, as well as solely with F. carica‎‎ leaf ‎‎extract, ameliorated both ‎the biochemical and histological indices of liver ‎damage. The findings suggest that the ‎methanolic extract of F. carica‎‎ leaves provides promising hepatoprotective effects against ‎CYP-induced liver damage in albino rats, likely via its antioxidative properties‎‎.

Phytochemical constituents of bark essential oils of Cinnamomum zeylanicum Blume and effects on liver tissue of rats

Cinnamomum zeylanicum Blume is an evergreen tropical tree belonging to the Lauraceae family; it is a useful plant in traditional and modern medicines. Essential oils of Cinnamomum zeylanicum were prepared and identified using gas chromatography–mass spectrometry (GC-MS). For histological study 80 adult male rats were employed in this study. It is the same weight (30 ±5 gm) and 75 days in age. The animals were divided into 4 groups, with ten rats in each group. The results indicated that C. zeylanicum bark contained 27 different phytochemical components. The main components included Cinnamaldehyde (2-Propenal, 3-phenyl-) (46.46%), 9-Methoxybicyclo, [6.1.0] nona-2,4,6-triene (31.31%), alpha-, Muurolene (7.14%) and Copaene (1.63%). Sections of livers were examined for histological abnormalities, such as the breakdown of the liver architecture and increased inflammation, in comparison to control samples, some hepatocytes were swollen with pyknotic, large nuclei and dilated sinusoids. As well as in the rats treated with noticed sever congestion of central vein (CV), degeneration and sluggish of endothelial lining larger, Bile ducts hyperplasia and necrotic hepatocytes. It can be deduced that the main component of cinnamon bark oil is cinnamaldehyde and the liver displayed some tissue changes, including hepatocyte necrosis and the existence of steatosis foci. Histological and cellular changes in liver tissue were dramatically attenuated by C. zeylanicum essential oil.

PROTECTIVE EFFECTS OF GRAPE SEED EXTRACT (VITIS VINIFERA) AGAINST CISPLATIN-INDUCED LIVER DAMAGE IN RABBITS. (HISTOLOGICAL AND HISTOPATHOLOGICAL STUDY)

Cisplatin is a chemotherapeutic drug used in the treatment of various cancer types. It can be considered a double-edged sword. It is a potent anticancer agent at the same time has toxic effect on various tissues as it causes hepatotoxicity. It was determined to cause liver toxicity and to weaken the antioxidant defense systems in liver. A decrease in antioxidant enzymes resulted from cisplatin induced tissue toxicity. Moreover, the development of therapies to prevent the appearance of cisplatin- induced tissue toxicities has focused on administration of antioxidants along with cisplatin treatment. The grape seeds exhibit a broad spectrum of pharmacological properties against oxidative stress. Therefore, the aim of present study was designed to investigate the protective effects of grape seed extract on the liver damage in cisplatin treated rabbits. Twenty seven healthy rabbits of local mixed breed were selected, divided into three equal groups, the first group (CON group) served as control and received a single intraperitoneal injection of normal saline solution once per week for 6 weeks; the second group (CIS group) were treated with therapeutic dose of cisplatin intraperitoneally once per week for six weeks; the third group (CIS+GSE group) served as protective group and was concomitantly treated with grape seeds extract by oral gavages and cisplatin injection intraperitoneally once per week for six successive weeks. Administration of grape seeds extract by oral gavages starting from the first day of the experiment for 6 consecutive days before and 6 consecutive days after the cisplatin injection and continued daily for 6 weeks. The histopathological findings present in current study showed that cisplatin toxicity produced significant structural changes in the liver of CIS group, cisplatin treated group, in the form of prominent disorganized architecture and loss of liver lobulation, distortion of the arrangement of parenchyma of the liver, loss of radial arrangement of sinusoids from the central vein of the liver, Dilatation and congestion of central veins, sinusoids and portal traids, degenerative changes in hepatocytes and pyknotic nuclei indicating necrosis. Marked vacuolar degeneration mainly hydropic ballooning degeneration and hyper activation of Kupffer cells and inflammatory cellular infiltrations were also observed. This finding reflected the cytotoxic effects of cisplatin in hepatic tissue. While, in the sections from the liver of animals received therapeutic dose of cisplatin and treated by grape seed extract, group (CIS+GSE) clearly showed that there was a significant alleviated hepatotoxicity, since histopathological changes were markedly less pronounced compared to animals treated with cisplatin alone. Therefore, and based on our findings, the grape seed extract contributes significantly to the improvement of histological alterations in rabbit liver caused by cisplatin.

The administration of oral mucosal mesenchymal-derived stem cells improves hepatic inflammation, oxidative stress, and histopathology following traumatic brain injury

BackgroundThe inflammatory mediators produced after traumatic brain injury (TBI) are reaching peripheral organs causing organ and tissue damage, including the liver. Our study assessed the effect of intravenous (i.v.) infusion of oral mesenchymal stem cells (OMSCs) on TBI-induced liver damage by measuring liver inflammatory factors and liver oxidative stress. MethodsTwenty-eight adult male Wistar rats were divided into four groups: 1) sham control; 2) TBI alone (TBI); 3) TBI vehicle (Veh)-control; and 4) TBI with OMSC treatment (SC). OMSCs were obtained from oral mucosa biopsies. OMSCs were administered and administered i.v. at 1 and 24 h after TBI. Within 48 h after TBI, multiple parameters were analyzed, including inflammation, oxidative stress, and histopathological changes. ResultsIn comparison to sham controls, the TBI alone showed in liver significantly increased levels of interleukin-1β (IL-1β; P < 0.001), interleukin-6 (IL-6; P < 0.001), malondialdehyde (MDA; P < 0.001), and protein carbonyl (PC; P < 0.001). At the same time the TBI alone decreased the liver levels of superoxide dismutase (SOD; P < 0.001), total antioxidant capacity (TAC; P < 0.001), catalase (CAT; P < 0.001), and interleukin-10 (IL-10; P < 0.001). In comparison to the TBI alone group, the therapeutic group treated with i.v. infusion of OMSCs demonstrated significantly reduced changes of IL-1β (P < 0.001), IL-6 (P < 0.01), MDA (P < 0.01), PC (P < 0.05), SOD (P < 0.001), TAC (P < 0.01), CAT (P < 0.01), and IL-10 (P < 0.01). Histopathological evaluation showed in TBI alone group that the total score of liver tissue injury included extensive hydropic degeneration, lobular necrosis, inflammation as well as central vein congestion with subendothelial hemorrhage increased compared the sham group (P < 0.001). Administration of OMSC showed significantly smaller increase in the injury score compared to the TBI alone group (P < 0.001). ConclusionTherapy with i.v. OMSCs administration after TBI reduces liver injury, as measured by inflammation and oxidative stress. The use of OMSCs can be considered for treatment of liver injury caused by TBI.

Paediatric pineal region cysts: enigma or impaired neurofluid system?

PurposePineal region cysts (PCs) may affect the tectum and aqueduct and cause deep central vein congestion. Beside headaches, PC often causes a broad range of symptoms, leading to prolonged diagnosis and therapy. The aims of this study are to reveal parameters that might explain the ambiguity of the symptoms and to identify factors in association with the respiration-driven neurofluid system.MethodsThis retrospective study included 28 paediatric patients (mean age 11.6 years) who received surgical treatment and 18 patients (mean age 11.3 years) who were followed conservatively. Symptoms, time to diagnosis, cyst size, ventricular indices, head circumference and postoperative outcome, were analysed. Four patients were investigated for CSF dynamics with real-time MRI. The mean follow-up time was 1.6 years.ResultsThe most common early onset symptoms were headaches (92%), blurred vision (42.8%), sleep disturbances (39.3%) and vertigo (32.1%). Tectum contact was observed in 82% of patients, and MRI examinations revealed that imaging flow void signals were absent in 32.1% of patients. The maximal cyst diameters were 13.7 × 15.6 mm (mean). Together with a postoperative flow void signal, 4 patients recovered their respiration-driven CSF aqueductal upward flow, which was not detectable preoperatively. After surgery the main symptoms improved.ConclusionDespite proximity to the aqueduct with frequently absent flow void signals, hydrocephalus was never detected. Data from real-time MRI depicted a reduced preoperative filling of the ventricular CSF compartments, indicating a diminished fluid preload, which recovered postoperatively.

Ameliorative effects of piroxicam on perchloric acid-induced thyroid gland hormones disruption in male rats

BackgroundThe incidence of goitre has increased world-wide, with African countries responsible for over 28 % of the cases. The danger of perchloric acid among males working in the factories has been on the increase. Hence mitigating effects of piroxicam on perchloric acid-induced thyroid hormones disruption was studied in male Wister albino rats. MethodsA total of 19 rats (17 males; 2 females) that weighed 145.0 ± 20.5 g were used for the.study. Four rats were used for determination of median lethal dose (LD50) of perchloric acid, whereas 15 rats divided into three groups of five each, were used for induction of thyroid hormones disruption, using 100 mg/kg of perchloric acid for a period of two weeks. Thereafter group II and III rats were treated with 2.5 and 5.0 mg/kg of piroxicam, respectively. Three millilitres of blood were collected from all the rats for determination of thyroid hormones, haematological and biochemical parameters. Brain, liver, spleen, lung, kidney and heart were harvested for allometry and histopathology. ResultsFindings have shown that LD50 of perchloric acid was 4207.5 ± 457.6 mg/kg body weight. Piroxicam significantly decreased (p < 0.05) thyroid stimulating hormone, but increased free triiodothyronine and thyroxine respectively. Alanine aminotransferase, aspartate aminotransferase, alkaline phosphatase and monocytes were increased significantly(p < 0.05). Urea, creatinine, haematocrit, erythrocytes, leucocytes, lymphocytes, neutrophils, platelets and eosinophils counts were decreased significantly (p < 0.05). Allometric parameters were significantly increased (p < 0.05). Histopathology revealed perivascular cuffs of brain, zenker’s necrosis with mononuclear cells infiltration of myocardium, congestion of central vein of liver, mononuclear cells infiltration of the kidney, lymphoid tissue aggregation of white pulp, congestion and thickness of the lungs were observed in the rats administered piroxicam. ConclusionHence piroxicam ameliorates thyroid hormones disruption, induces liver enzymes, modulates humoral immune system, enhances renal function and decreases allometric parameters of brain, lung and liver, as evidenced by histopathological lessons.

The Preclinical Benefit of Glutamine in bisphenol A-induced Hepatotoxicity in Wistar Rats

Background: Oxidative stress may be a causative factor for bisphenol A (BPA) -induced hepatotoxicity. Glutamine (GM) is an amino acid with the ability to inhibit oxidative stress. Objective: This study evaluated the ability of GM to prevent BPA-induced hepatotoxicity in rats. Methods: Adult Wistar rats of both sexes (n=30) were used. The rats were randomly grouped into six of five rats each. Groups A (Control), B, and C were treated with normal saline (0.2 mL), GM (80 mg/kg), and BPA (50 mg/kg), respectively for 60 days. Groups D-F were treated with GM (20 mg/kg)+BPA (50 mg/kg), GM (40 mg/kg)+BPA (50 mg/kg), and GM (80 mg/kg)+BPA (50 mg/kg), respectively for 60 days. After treatment, blood and liver samples were obtained for biochemical and histological assessments, respectively. Results: Significantly (P&lt;0.01) decreased body weight and significantly (P&lt;0.01) increased liver weight occurred in the BPA-administered group when compared to the control group. The BPA-administered group showed significantly (P&lt;0.001) elevated serum total bilirubin, lactate dehydrogenase, aminotransferases, conjugated bilirubin, gamma-glutamyl transferase, alkaline phosphatase, and liver malondialdehyde concentrations when compared to the control group. Significantly (P&lt;0.001) decreased liver superoxide dismutase, glutathione peroxidase, catalase, and glutathione levels occurred in the PBA-administered group when compared to the control group. BPA caused hepatocyte necrosis, sinusoids, and central vein congestion. BPA-induced hepatotoxicity was reversed by GM; 20 mg/kg (P&lt;0.05), 40 mg/kg (P&lt;0.01), and 80 mg/kg (P&lt;0.001) in a dose-related fashion when compared to BPA. Conclusion: GM may be effective against BPA-associated hepatotoxicity.

STUDY SOME PHYSIOLOGICAL ASPECTS AND HISTOPATHOLOGICAL CHANGES IN MALE RABBITS INTOXICATED BY CHLORPYRIFOS

The current experience on chlorpyrifos was undertaken to investigate the potential alterations in Physiological Criteria and in liver and kidney tissues subsequent oral exposure of chlorpyrifos in male rabbits . twelve of male rabbits were employed in this experience, distributed into two groups randomly , group one received only corn oil and served as control, whereas, while group two received CPF 33.3 mg/kg dissolved with( 1ml ) corn oil daily, the exposure continued for 28 consecutive days orally. outcomes of this work revealed that sub-acute oral administration of chlorpyrifos cause to oxidative stress evidenced by pronounced elevation value of oxidative biomarker malondialdehyde ( MDA) concomitantly with elevated in values of inflammatory biomarkers ( TNF-α and CRP) and significantly reduction in total antioxidant capacity (TAC) value, as well as this findings exhibited that chlorpyrifos administration cause to marked alteration of blood indices values as well as histopathological changes were observed in liver and kidney which as represented degenerative of hepatocyte, dilatation and congestion in central vein, While tubular epithelial degenerations, vacuolations and severe dilation in renal cortex tubules. Conclusion: we concluded from findings in this study the oral exposure to CPF evoked inflammation response and oxidative damage as represented by pronounced elevation in levels of CRP,TNF-alpha and MDA biomarkers as well as pathohistological alterations were observably in liver and kidney that indicating that chlorpyrifos elicits numerous adverse effects noteworthy making it a major public health issue.

Antiplamodial effect of sulfadoxine/pyrimethamine/clindamycin: A study in parasitized mice

Triple antimalarial combination therapies may overcome the emergence of antimalarial drug resistance. Sulfadoxine/pyrimethamine (S/P) is an antimalarial drug. Clindamycin (C) has potential antiplasmodial effect. This study assessed whether the antiplasmodial activity of S/P can be augmented by C on Plasmodium berghei-infected mice. Adult Swiss albino mice (25-30g) were grouped and infected with Plasmodium berghei. The mice were orally treated daily with S/P (21.4/10.7 mg/kg), C (10mg/kg) and S/P/C, respectively using curative, prophylactic and suppressive tests. The normal and negative controls were treated daily with normal saline (0.2mL) while the positive control was orally treated with chloroquine (CQ) (10mg/kg). After treatment, blood samples were collected and evaluated for percentage parasitamia and hematological parameters. Mice were observed for mean survival time. In the curative, suppressive and prophylactic tests, S/P/C significantly decreased parasitamia levels when compared to SP or C at p&lt; 0.05. S/P/C significantly prolonged mean survival time when compared to S/P or C with difference at p&lt; 0.05. S/P, C, and S/P/C produced 65.62 %, 62. 03 % and 85.31 % parasitamia inhibitions, respectively while CQ produced 83.72 % parasitamia inhibition. S/P/C caused significant reduction in anemia marked by increased packed cell volume, hemoglobin, red blood cells and decreased white blood cells at p&lt; 0.05 when compared to SP or C. S/P/C eradicates liver merozoites and central vein congestion. C increased the antiplasmodial activity of S/P, therefore S/PC may be used for malaria treatment.

Morphological changes in liver of wistar rats induced by Gold Kushta

Objective: To observe hepatic changes induced by Gold Kushta. In our study the histopathological effects of Gold Kushta was seen in livers of Wistar rats. Study Design: Experimental study. Setting: Department of Pathology, Sahiwal Medical College, Sahiwal. Period: 1st July 2019 to 31st Dec 2019. Material &amp; Method: Total of 28 wistar rats of 6 – 8 weeks of age and weighing 200 – 250 grams which were then randomly divided into 4 groups each containing 7 rats. The groups were labelled as G I, II, III and IV. These groups were given preparations of gold in the form of kushta for a period of 8 weeks. The gold kushta was given in the form of pellets. Group I was taken as Control, G II was given single dose kushta 0.15 mg and G III was given double dose kushta 0.3mg on alternate days. Group IV was given a single dose of BSA (bovine serum albumin) 75mg (250mg/kg body wt) at the start of experiment and Gold kushta 0.3 mg on alternate days. Histopathological changes were then seen in lobules, sinusoids, kupffer cells and central veins of livers of wistar rats. Results: The histological examination of liver showed sinusoidal congestion and central vein congestion, apoptosis, necrosis and hydropic degeneration as common features. In addition fatty degeneration, inflammation and kupffer cell hyperplasia were also seen in few cases. These changes were observed in all the above groups except group G I serving as control. More changes were seen in high dose groups and the groups given BSA inj. (Group II, III and IV). Conclusion: Thus, indigenous preparations of gold kushta have detrimental effects over livers of wistar rats and are thus hepatotoxic.

Protective Effect of Pyridoxine on Lead Nitrate Induced Histomorphological Changes in Rat Liver

Objective: To study the effects of Pyridoxine on lead nitrate generated histological and morphological changesin rat liver.Study Design: It was an experimental study.Place and Duration of Study: The study was carried out at Anatomy Department of College of Physicians andrd st Surgeons, Islamabad, Pakistan from 03rd September, 2019 to 31st December, 2020.Materials and Methods: In this study 90 male rats were used and divided into three groups. Control group Awas kept on normal diet. Experimental group B1 was given lead nitrate and B2 was given lead nitrate andpyridoxine by oral gavage for a period of 2 weeks. All rats were sacrificed after 2 weeks. Results of quantitativevariables such as inflammatory and Kupffer cells were expressed in mean ± S.D. To detect significant differenceamong the groups, ANOVA accompanied by Post Hoc Tukey test was applied and qualitative data such as central vein congestion, steatosis, and necrosis were expressed in percentages and Chi Square test.Results: Exposure to pyridoxine reduces the degenerative changes caused by lead nitrate such as increase inthe number of Kupffer and inflammatory cells. Central vein congestion, steatosis and necrotic foci were alsoreduced with a significant p-value.Conclusion: An ameliorative effect of pyridoxine on the degenerative changes in the liver induced by leadnitrate was proven through a decrease in the number of kupffer and inflammatory cells. Central veincongestion, steatosis and necrotic foci were also reduced significantly.&#x0D; How to cite this: Abbasi S, Khan HM, Khan MY. Protective Effect of Pyridoxine on Lead Nitrate Induced Histomorphological Changes in Rat Liver. Life and Science. 2022; 3(4): 163-167. doi: http://doi.org/10.37185/LnS.1.1.269

A histopathological study on the effects of cyclophosphamide on the hepatic tissue of female golden hamsters

The aim of this study was to study the acute toxic effect of cyclophosphamide on the histological structure of the liver tissue in Syrian golden hamsters. Twenty-seven adult female hamsters were injected intraperitoneally with 0, 100 and 200 mg/kg body weight cyclophosphamide. The dosing was administrated on alternating days for one week as an acute dosing schedule and humane sacrifice was done on day 7. Hepatic tissue was collected and processed with paraffin technique for histological examination then stained with hematoxylin and eosin stains (H&amp;E) and Periodic acid–Schiff stain (PAS). The control tissues showed normal histological structure of the liver tissue. With H&amp;E histological changes appeared in the tissue from the hamsters dosed with 100 mg/kg body weight in the form of; slight fatty changes with vacuolated cytoplasm in some areas. The higher dose showed diffuse fatty infiltration, central vein congestion and loss of hepatocyte architecture in addition to sinusoidal congestion. With PAS stain for both low and high doses showed a decrease in glycogen amount due to presence of degenerative hepatocytes and necrosis. We recommend for the patients who undergo long term therapy with cyclophosphamide to perform clinical and biochemical tests at regular intervals to indicate early on any hepatic dysfunction.

Excessive Green Tea Intake Alters Hemoglobin (Hb) Concentration and Histoarchitecture of Liver

A myriad of health claims are being made in favor of the consumption of green tea due to its easy availability and greater popularity. On the contrary, certain health risks of excessive green tea consumption have begun to emerge. The aim of the present research was to observe the baleful effects of excessive green tea intake on hematological parameter and histoarchitecture of liver. A total of thirty (n=30) Swiss albino mice were taken and randomly divided into Control C, Treated T1, and Treated T2 groups. Each group consisted of ten (5 male+5 female) mice. The Control C group was fed with normal mice pellet and water (3ml/mice) orally but the treated T1 group was supplied mice pellet with 2ml/mice of green tea+1ml/mice of water orally as well as treated T2 group was given mice pellet and 3ml/mice of green tea orally two times in a day for 60 days. After the experimental tenure, mice of each group were sacrificed ethically and samples (Blood, liver and lungs) were collected for further hematological and histomorphological studies. Treated T2 group of mice were motionless (inactive and stagnant). Anatomopathologically, the liver surface became dark red in color with considerable hepatomegaly and mild hemorrhage also found on lung surface. Histologically, mild central vein congestion and severe venous congestion with dilation were found in the portal vein of the liver of the treated T2 group of mice. Hematologically, hemoglobin level significantly reduced in the treated T2 group of mice than the others. Within this experimental period, female mice of each group gave birth (15-18 pups) that were devoid of any abnormality. Therefore, it can be concluded that excessive green tea intake in a day might have baleful effects on hematological parameter (Hb concentration) and histoarchitechture of liver in Swiss albino mice.

Bisphenol S induced dysregulations in liver; iron regulatory genes and inflammatory mediators in male Wistar rats.

Bisphenol S (BPS), an analog of bisphenol A (BPA), has been frequently detected in consumer products, food wrappers, plastics, and thermal papers. Since the liver is a hub of metabolic and detoxification pathways, thus intimately related to BPS presence in the environment and body. The current study was designed to investigate the effects of BPS administration in an animal model. Twenty-five male Wistar rats weighing 175 ± 25 g were randomly divided into control and treated groups. The control group was further divided into group I (no treatment) and group II (corn oil), whereas the treatment group was divided into D-I (40 mg/kg/day), D-II (200 mg/kg/day), and D-III (400 mg/kg/day) groups, getting oral doses of BPS for 15 days. Data analysis showed a significant statistical increase in hepatic enzymes ALT (33.4%), AST (25.4%), and ALP (529.6%) in the D-III group along with the development of hypercholesterolemia and hypertriglyceridemia in all BPS groups. Aberrant mRNA expressions of some key hepatic iron regulatory genes and inflammatory mediators were evident through qRT-PCR. Bisphenol S caused congestion of central vein from mild to moderate in hepatic sections. In conclusion, our investigation insinuates BPS intoxication potential and therefore may not be a safe alternative to BPA.

Investigation on Immune-Related Protein (Heat Shock Proteins and Metallothionein) Gene Expression Changes and Liver Histopathology in Cadmium-Stressed Fish.

Heat shock proteins (HSP) are highly conserved in their structure and released in case of stress. Increased metallothionein (MT) synthesis is associated with increased capacity for binding heavy metals. Healthy juveniles of grass carp were exposed to sublethal dose (1.495 mg L−1) of cadmium for 28 days. Simultaneously, a control group was also run to compare difference of total RNA expression levels in cadmium-treated and control groups. The cadmium levels in the tissues of treated fish recorded were 1.78 ± 0.10 mg L−1, 1.60 ± 0.04 mg L−1, and 2.00 ± 0.05 mg L−1, respectively. Several histological alterations including edema, hemorrhage, dilated sinusoids, hypertrophy, hyperplasia, congestion of central vein, and nuclear alterations were observed in cadmium-exposed fish. Stress gene (metallothionein and heat shock proteins) mRNA transcription levels were studied by mRNA extraction and cDNA preparation by using PCR. The expression level of heat shock protein gene was higher as compared to metallothionein and beta-2-microglobulin gene after cadmium exposure. This study reports various stress-related immune-responsive changes of immune proteins, heat shock proteins, metallothionein, and histopathological changes in fish due to cadmium toxicity that make the fish immunocompromised which may be considered as the biomarkers of cadmium toxicity in other experimental species.

Chronic Antidepressant Use

Background: Chronic use of antidepressant drugs often results in drug-induced organ damage, which is mostly undetected and under-reported. The study aimed at evaluating the effect of selected antidepressants on organs and blood cell counts in adult albino rats. Materials and Methods: Adult rats were divided into four groups (n = 5): Group 1 (5 mL/kg of body weight/day normal saline), Group 2 (1 mg/kg of body weight/day risperidone), Group 3 (5 mg/kg of body weight/day fluoxetine), and Group 4 (15 mg/kg of body weight/day imipramine) for 14 days. The animals experienced different stressors during the treatment period to simulate physiological state of depression. On the 14th day, the animals were exposed to the forced swimming test 1 h after the respective treatments. On the 15th day, the animals were sacrificed under halothane anesthesia. Blood sample was collected. Liver and kidney were excised for histological examination. Results were analyzed using one-way analysis of variance. Results: Kidney histology was normal for all groups. Risperidone-exposed rats presented with hepatotoxicity with areas of zonal necrosis and partial central vein congestion. Neutrophil (%) was significantly reduced (P &lt; 0.01) in all treatment groups when compared with controls. White blood cell count was significantly increased (P &lt; 0.01) in the imipramine and risperidone treatment groups but significantly reduced (P &lt; 0.01) in the fluoxetine treatment group when compared with controls. Also, the platelet count was significantly increased (P &lt; 0.01) in the fluoxetine group but decreased in imipramine-and risperidone-treated groups. Conclusion: Chronic antidepressant use can cause changes in blood cell counts and drug-induced organ damage; hence, frequent organ function tests and blood count are required in patients undergoing chronic antidepressant therapy.

Effects of Lead Nitrate Induced Histological Changes in Liver of Male Sprague Dawley Rats

Lead is a highly toxic agent and a potent risk factor for various diseases as its quantity in an environment is increasing day by day. Aim: To observe and analyze the lead nitrate induced histomorphological changes in the liver of Sprague Dawley rats. Study Design: Experimental Study. Methodology: Animals of group A (control) were fed on normal diet but the animals of group B were given 50mg/kg of lead nitrate dissolved in 10ml of distilled water through oral gavage for 14 days daily. SPSS version 22 was used for data analysis. All the quantitative data was expressed as means ± SD. One Way ANOVA followed by Post Hoc Tukey test was applied. Results: Degenerative effects were noted. The number of Inflammatory and Kupfffer cells is increased with decreased in the body weight. Steatosis and central vein congestion were also present. Conclusion: It was concluded that degenerative effects histologically may be due to oxidative stress produced by formation of free radicals and denaturation of proteins by lead nitrate. Keywords: Lead, Liver, Central Vein Congestion, Oxidative Stress and Free Radicals.

The Effect of Pseudoephedrine (Sudafed) on Kinetic activity and histology of Livers and Kidneys in Albino Mice

Pseudoephedrine (PSE) or (Sudafed) is one of the sympathomimetic group of drugs (ephedrine, PSE and amphetamines) which effects cardiovascular system, respiratory system, and gastrointestinal tract. However, only little researches had supported its effect on solid abdominal organs. This study aims to investigate the effects of different doses of Sudafed in the liver and kidney of albino mice. The current study included 18 albino mice grouped into 2 groups: control (3 mice), and acute group (15 mice). The acute group was further subdivided into 5 subgroups, each subgroup of 3mice wasgiven a lonely intaperitonial injection of 0.3ml of the following conc. (500mg/kg, 250mg/kg, 125mg/kg, 62.52mg/kg, and 31.24mg/kg) for 24hrs. After the mentioned period, the mice of all subgroups were sacrificed and the livers and kidneys were removed, processed, sectioned and stained for histological analysis. Results of liver analysis using 500mg/Kg Sudafed intraperitoneallyshowed mild ballooning degeneration of hepatocytes and central vein congestion, while lower doses (250mg/Kg – 31.42mg/Kg) revealed less prominent effect or no significant pathological changes.Moreover, sections from the kidney with the 500mg/Kg Sudafed intraperitoneally showed mild hydropic swelling of tubular epithelium with congestion of intertubular blood vessels and relatively healthy glomeruli. Lower doses revealed no significant pathological changes. Conclusion: The present study demonstrated various pathological effects of PSE on kinetic activity, and histology of Livers and Kidneys of albino mice.