Protective effect of Kappaphycus alvarezii (Rhodophyta) extract against DNA damage induced by mercury chloride in marine fish

Marine organisms are continuously exposed to agents, both exogenous and endogenous, that damage DNA. Consequently, it is important to determine the ability of compounds to provide protection against damaging chemicals. The aim of this study was to evaluate the anti-genotoxic activity of crude aqueous extracts of Kappaphycus alvarezii (Rhodophyceae), collected from the Southeast coast of India. This study focused on possible anti-genotoxic potential of aqueous extract of K. alverazii to interfere with clastogenicity induced by mercury chloride (HgCl₂) in marine fish, Therapon jarbua as measured by cytogenetic endpoints such as cell viability and comet assay. In the first set of experiments, fish were exposed to a single treatment of Hg at 0.125, 0.25, 0.5, 1, or 2?ppm along with controls. Mercury exposure produced significant DNA damage in all comet classes, maximum as >79% (Class 4) at 0.5, 1, and 2?ppm exposure in a time dependent manner. Algal extract did not induce genotoxicity when given alone and prevented Hg-induced genotoxicity. The algal extract reduction in genotoxicity was significant but not time- and concentration-dependent. Results suggested that under present experimental conditions, K. alvarezii extract exhibit potent anti-genotoxicity effects in this fish model; and thus these extracts may be recommended as a supplement in fish meal and may benefit humans ingesting Hg-contaminated fish.     

Zinc induced histological changes in brain and liver of Labeo rohita (Ham.)

Labeo rohita fingerlings were exposed to zinc metal toxicity (5 and 10 ppm) for duration of 5 and 15 days. The histological changes were studied in brain and liver of the treated fish. The brain tissues showed enlarged pyramidal cells with extensive vacoulation while severe necrosis, haemorrhage and degeneration of hepatocytes were witnessed in the liver tissues.     

Histopathological impact of industrial wastewater on the vital organs of Oreochromis mossambicus

The acute toxicity of paper mill wastewater to Oreochromis mossambicus was investigated with the lethal concentration (LC50) value 6.5% for 96?h exposure. This concentration was used as a baseline to study the effects of paper mill effluent on histopathological changes in gills, liver, kidney, and brain of fish. In the gills, filament cell proliferation, cellular infiltration, hemorrhage, and epithelial lifting were observed. In the liver, vacuolation of hepatocytes and necrosis were noted. In kidney, exfoliation and swollen with pyknotic nuclei were identified. Similarly, the brain also showed enlarged pyramidal cells, binucleated nuclei, vacoulation, and necrosis. These changes occurred predominantly in 21days following exposure of fish to the industrial waste water. Paper mill wastewater was found to be highly toxic to fish.     

Lead- and cadmium-induced histopathological changes in gill,kidney and liver tissue of freshwater climbing perch Anabas testudineus (Bloch, 1792)

The objective of this study was to examine the toxicological effect of two major heavy metal pollutants, lead chloride (PbCl₂) and cadmium chloride (CdCl₂), in the freshwater climbing perch, Anabas testudineus. Fish were exposed to 1.0 and 2.0 mg/L both metals and histopathological changes in gill, kidney and liver tissues were studied. Major changes observed in gill tissue were epithelial lifting, proliferation of epithelial cells, fusion of secondary lamellae, hyperplasia and hypertrophy of mucous cells, and necrosis of epithelial cells. Cell necrosis, degenerated kidney tubules, congestion, lymphocytic infiltration and vacuolation were the major abnormalities observed in kidney tissue. The most conspicuous changes in liver were darker nucleoli, irregularly shaped hepatocytes with dilated blood capillaries, and focal as well as single necrosis. Fish specimens exposed to PbCl₂ exhibited pronounced changes in all tissues examined compared with those exposed to CdCl₂. It is evident from this study that heavy metals can cause significant histopathological changes in fish tissue.     

Effects of UV-B radiation on the gills of Catla catla during early development

Scanning electron microscopic (SEM) study of gills of Catla catla catla (17-day-old) exposed to UV-B radiation (145?µW?cm^?2 at the water surface) for three different exposure times: 5, 10 and 15?min was conducted. Fish without UV-B exposure served as control. UV-B radiation damaged both gill filaments and lamellae. The intensity of damage was minimal in 5?min exposed fish, followed by 10?min exposed fish and maximal in 15?min. The gill epithelium was severely damaged in 15?min irradiated fish compared to control. Pavement cells (PVCs) were damaged and the numbers of microridges within PVCs decreased. The deep boundary of PVC was not clear. In some area of gill epithelium, PVCs were destroyed and mitochondrion-rich cells (MRCs) were exposed. The 5?min exposure reduced the number of microridges in the PVCs, but the boundary of PVCs was still visible. MRCs in the gill epithelium were not exposed in 5?min exposed fish. The damage to PVCs and subsequent exposure of MRCs in UV-B irradiated fish may hamper respiratory functions and disturb osmoregulation in catla.     

Influence of marine alga against mercury-induced biochemical changes,structural destabilization,and genotoxicity in marine tiger fish,Therapon jarbua

This study elucidated the protective role of alga against mercury (Hg)-induced toxicity in marine fish. Bath immersion with mercury chloride (HgCl) [0.125 and 0.25?ppm] in combination with the algal extract (3?ppm) to Therapon jarbua offered a significant protection against Hg only induced disturbed liver function, damaged histoarchitecture, elevated oxidative stress, and DNA fragmentation of tissues. Mercury exposure decreased hepatic superoxide dismutase (SOD), catalase (CAT) activities, and the level of nonprotein-soluble thiol (NPSH, GSH), with a concomitant increase in thiobarbituric acid reactive substances (TBARS) in the gill, kidneys, liver, and blood. Algal supplementation diminished the rise in TBARS restoring CAT, SOD, and GSH levels to control. Reduced generation of free radicals may be correlated to protect DNA stability and morphology. This study indicates the ability of alga to ameliorate Hg-mediated injuries. In conclusion, Kappaphycus alvarezii extract did not show any toxicity and its safety is suggestive for using as a supplement in fish food.     

Histological and histochemical alterations induced by lead in the liver of the quail Coturnix coturnix

Adult males of the quail Coturnix coturnix were exposed to lead acetate trihydrate in drinking water (0.1, 0.25, 0.5, and 1% for one–six months) to investigate histological and histochemical alterations induced by lead intoxication in the liver. Chronic exposure to subtoxic concentrations of lead produced changes in hepatocytes, portal veins, Kupffer cells, and blood sinusoids. Alterations in hepatocytes mainly involved cytoplasmic vacuolation, necrosis, cytolysis, and glycogen accumulation. Kupffer cell hyperplasia, hemosiderosis, blood sinusoidal dilatation, portal vein congestion, and edema were also observed. No fibrosis or cirrhosis in the liver of any member of the dose groups over the entire period of the study was noted. The findings revealed that chronic exposure to lead produced mild histological and histochemical changes in the liver of the quail Coturnix coturnix.     

Effects of organochlorines on the ultrastructure of the liver of the damselfish Parma microlepis from reefs in New South Wales, Australia

  Parma microlepis (Günther) were collected from Malabar, an urban location close to the centre of Sydney, Australia, and from Jervis Bay, a reference location 170 km south of the city centre. At each location, fish were collected from two sites separated by 100 to 200 m. The ultrastructure of normal liver tissue is described based on 20 female fish collected from Jervis Bay, where fish are known to be exposed to low levels of organochlorine contaminants. Alterations in the endoplasmic reticulum, mitochondria, lysosomes and nuclei of hepatocytes were identified and quantified in the liver tissue of fish from this location and compared to alterations in 20 female fish collected from Malabar, where fish are exposed to higher concentrations of organochlorine pesticides such as DDT compounds. There were significant differences in the percentage of hepatocytes with swollen mitochondria (F = 124.025, df = 2, 2, P = 0.008) and atypical nuclei (F = 22.198, df = 2, 2, P = 0.043) between sites (100 to 200 m apart), but there were no clear differences between the percentage of structural alterations in the hepatocytes of P. microlepis from Jervis Bay and Malabar. Associations between liver morphology and the organochlorines aldrin, dieldrin, DDE and chlordane were examined using a Pearson correlation matrix. Significant correlations were detected between the percentage of hepatocytes with dilated endoplasmic reticulum and the concentrations of the pesticide aldrin (r = 0.600, df = 11, r _{crit(α = 0.05)} = 0.553). Significant associations were also detected between the percentage of hepatocytes with disorganised endoplasmic reticulum and the concentrations of dieldrin and DDE residues in fish (r = 0.576, r = 0.567, respectively, df = 13, r _{crit (α = 0.05)} = 0.514). However, there was little evidence that ultrastructural alterations in fish responded to increasing concentrations of these pesticides in a consistent dose-response manner. Received: 20 October 1998 / Accepted: 24 November 1999     

林丹短期暴露下的斑马鱼(Brachydanio rerio)组织学变化

以斑马鱼(Brachydaniorerio)为受试生物,初步探讨了林丹对斑马鱼的急性毒性以及不同浓度(0.01μg·L-1、1.0μg·L-1、100.0μg·L-1)的林丹暴露36d后对斑马鱼鳃和肝组织结构变化的影响.结果表明,林丹对斑马鱼96h-LC50为97.98μg·L-1,95%可信限为94.38￣101.72μg·L-1.当林丹浓度为0.01μg·L-1时,斑马鱼的鳃和肝组织结构未发生明显变化,而暴露在1.0μg·L-1和100.0μg·L-1林丹溶液中的斑马鱼的鳃和肝组织结构变化显著.斑马鱼鳃组织变化为:上皮细胞残损、脱落,鳃小片上皮细胞水肿,柱细胞变形.斑马鱼肝组织变化为:部分肝细胞肿大,细胞核萎缩变形或偏离细胞中心,胞质疏松,空泡明显增加,细胞质中可见脂沉积.与1.0μg·L-1林丹暴露相比,暴露在100μg·L-1林丹溶液中的斑马鱼鳃和肝组织结构受到的损害更为严重.     

Comparison of cellular and molecular cytotoxic mechanisms of Cochlodinium polykrikoides in isolated trout and rat hepatocytes

Harmful algal blooms produced by the marine ichthyotoxic dinoflagellate Cochlodinium polykrikoides are responsible for mass mortalities of wild and farmed fish globally. This study compared the cytotoxic mechanisms of C. polykrikoides total extract on both trout and rat liver hepatocytes. Trout hepatocytes were more sensitive than rat hepatocytes against C. polykrikoides extract. The effective concentration 50 after 3 hour incubation (EC50_3hr) concentrations found for C. polykrikoides extract in trout and rat hepatocytes (i.e., 50% membrane lysis in 3 hr) were Eq. 1 cell/ml and Eq. 240 cell/ml, respectively. C. polykrikoides extract exposure in both isolated trout and rat hepatocytes resulted in membrane lysis, reactive oxygen species formation, glutathione depletion, collapse of mitochondrial membrane potential, ATP depletion, increase in adenosine diphosphate (ADP)/adenosine triphosphate (ATP) ratio, cytochrome c release into the hepatocyte cytosol, and activation of caspases cascade. Trout hepatocyte toxicity was also associated with lysosomal membrane injury. Mitochondrial permeability transition in both trout and rat hepatocytes produced cytochrome c release from the mitochondrial intramembrane space into the cytosol. Thus, the cytochrome c release triggered activation of caspase-3 and apoptosis. Finally, data demonstrated that C. polykrikoides extract may induce more apoptotic phenotype in rat than trout hepatocytes, which in the latter favored predominantly necrotic mode of cell death.     

Neurotoxin-induced cardiac disorder and its role in the death of fish exposed to Chattonella marina

This study was carried out in July 1989 and 1990 to confirm whether the neurotoxins of the red tide organism Chattonella marine contribute to the cardiac disorder and death of fish. Exposure of fish to C. marina red tide water significantly decreased the heart rate, presumably resulting in anoxia from reduced blood circulation in the gill. Since atropine restored the depressed heart rate, the cardiac disorder seemed to occur neurogenously in association with the intrinsic cardiophysiology of the fish. Neurotoxin fractions of C. marina and Gymnodinium sp. depolarized the vagal nerve of fish, and hence induced the reduction of heart rate. Depression of the heart rate in fish exposed to C. marina red tide water, thus, seemed to be caused by the neurotoxins of these organisms. Histological examination showed little branchial damage due to neurotoxin fractions.     

Oxidative stress and changes in locomotor behavior and gill morphology of Gambusia affinis exposed to chromium

Sublethal effects of chromium trioxide on mosquito fish, Gambusia affinis, were carried out for 28 days on day 4, 8, 12, 16, 20, 24, and 28. The sublethal effects of chromium (LC₁₀, 77.62?mg?L^?1) on antioxidant enzymes, thiobarbituric acid reactive substance (TBARS), locomotor behavior, and gill morphology were studied. The antioxidant enzymes like superoxide dismutase (SOD) and catalase were induced throughout the exposure span of 28 days. Percent induction was also increase with the days of exposure. Lipid peroxidation product, malondialdehyde was enhanced in the viscera tissue of chromium-exposed fish. Perturbation of locomotor behavior like decrease in distance travelled (m?min^?1) and in swimming speed (cm?s^?1) was observed in exposed fish. Chromium toxicity caused alterations in gill morphology like hypertrophy and hyperplasia in secondary lamellae followed by detached epithelium with severe necrosis. It can be concluded from the results that Cr intoxication in Gambusia fish, caused induction in antioxidant enzymes and lipid peroxidation, plus changes in gill morphology and locomotor behavior.     

Biomarkers of oxidative stress as indicators of water pollution in Nile tilapia (Oreochromis niloticus) from a water reservoir in Riyadh,Saudi Arabia

Antioxidant enzyme activities of fish (Oreochromis niloticus) were determined in order to assess the status of pollution in the Wadi Namar (WN), near Riyadh, Saudi Arabia. Activities of four antioxidant enzymes as superoxide dismutase (SOD), catalase (CAT), glutathione S-transferase (GST), and concentrations of glutathione (GSH) and oxidant malondialdehyde (MDA) were selected as bioindicators. Fish (n = 14) were sampled in the month of April 2013 from WN and a control site (CS). SOD activity was increased by 37.9%, 47%, and 29% in kidney, liver, and heart, respectively, while a significant decrease (36.4%) was observed in gills of O. niloticus from WN as compared to fish from CS. CAT activity was reduced by 51%, 55%, 47%, and 35% in kidney, liver, heart, and gills of O. niloticus from WN. The GST activities in kidney, liver, and heart of O. niloticus from WN were elevated by 34%, 48%, and 32%, respectively. However, significant fall (49%) in gills of fish was noted from WN compared to fish from CS. GSH levels were increased by 44%, 36%, and 38% in kidney, liver, and heart, respectively, but decreased by 30% in gills. MDA levels of O. niloticus were significantly increased in kidney, liver, and heart in fish from WN. Data indicated that WN is polluted mainly by industrial and urban discharge of liquid waste products.     

Structure of and energy reserves in the liver of wild and cultured yellowtail flounder,<Emphasis Type="Italic"> Limanda ferruginea</Emphasis>

Knowledge of the structure and energy reserves, in the liver of commercially important fish species, is important in understanding metabolic processes and in assessing the impact of potential environmental physical and chemical stressors in both wild and cultured stocks. The present study investigated the microscopic morphology and histochemistry (total and neutral lipids, glycogen) of liver tissue of wild (3 ⁺) and cultured (1 ⁺) sexually immature female and male yellowtail flounder ( Limanda ferruginea Storer), sampled in late April 2001. Hepatosomatic indices [HSI: (liver weight/body weight-liver weight)×100] of cultured fish were significantly higher than those of wild fish. Females in the cultured group had significantly lower HSIs than males. The liver of both wild and cultured L. ferruginea was interspersed with pancreatic tissue. The main components of the liver tissue were irregular cords of hepatocytes arranged in tubules which surrounded vascular sinusoids. The hepatocytes contained an abundance of lipid, much of which appeared to be neutral lipids, in both sexes of the cultured fish. Total and neutral lipid droplets were larger, and the area occupied by these droplets was significantly greater in both cultured females and males compared to the wild fish, suggesting lipidosis in the cultured fish. In the cultured fish these differences were sex-dependent, the females having significantly more total and neutral lipids in hepatocytes than the males. This suggests a potentially greater storage capacity in females and/or a higher lipid metabolism in males. There were no statistically significant differences in glycogen content between the cultured and wild fish, or between the sexes in both sampling groups.     

铜在日本青鳉体内的累积特征及其对肝脏组织结构的影响

为了解水体铜(Cu(Ⅱ))在日本青鳉(Oryzias latipes)脑、鳃、肝脏、性腺和肌肉组织中的累积特征,以及Cu(Ⅱ)对肝脏组织结构的影响,本文采用生态学单因子梯度实验,进行20 d的日本青鳉毒性暴露试验。结果显示,日本青鳉各个组织对Cu(Ⅱ)的累积量随着浓度的升高而增多,但不同组织对Cu(Ⅱ)的累积量有较大的差异,铜累积量由大到小依次为:肝脏脑鳃性腺肌肉。铜暴露后的日本青鳉肝细胞出现肿大、大小不一、排列混乱,静脉扩张淤血,部分肝细胞固缩和坏疽等现象。肝脏是日本青鳉蓄积铜的主要器官之一,实验发现高浓度的Cu(Ⅱ)对肝脏组织结构造成了明显的损伤,进而严重影响日本青鳉的存活率。     

Pathological effects of sublethal diazinon on the blood,gill, liver and kidney of the freshwater fish Capoeta damascina

Capoeta damascina has a large distribution in the Middle East and is one of the most abundant fishes in inland waters of Iran. Histopathological symptoms of the blood, gill, liver and kidney of C. damascina were investigated over 1, 5 and 9-day exposure to 0 (control), 0.5, 1 and 1.5?mg?L^?1 diazinon. The data were analysed using analysis of variance and non-parametric multivariate analysis of variance. Diazinon concentration was more important than the exposure time on changes of the tissues. Diazinon decreased red blood cell (RBC), white blood cell (WBC), haematocrit (Hct) and haemoglobin (Hb). The symptoms of the gill were mainly desquamation, epithelial hyperplasia, hyperplasia at the base of secondary lamella, epithelial lifting and curling. The prevalent symptoms of the liver were degeneration of nuclei, alternation in size and shape of hepatocytes, focal necrosis and pyknosis. Degeneration of Bowman's capsule, necrosis in renal tubule and haematopoietic tissue were the most common symptoms found in the kidney. In conclusion, the blood, gill, liver and kidney of C. damascina are sensitive enough to respond to low concentrations of diazinon over a short period and this species can thus be a bioindicator of diazinon.     

Determination of cytotoxic,genotoxic, and oxidative damage from deltamethrin on primary hepatocyte culture of Lake Van fish,Alburnus tarichi

ABSTRACT

Deltamethrin is a widely used pyrethroits worldwide. Although the chemical is used to combat insects, it has effects on other non-target organisms. Deltamethrin is extensively used in agriculture, animal husbandry, and domestic areas in the Lake Van basin. The aim of this study was to determine the cytotoxic, genotoxic, and oxidative damage from deltamethrin on the primary hepatocyte culture of Lake Van fish (Alburnus tarichi). In this study, the toxic effects of different concentrations (0.01, 0.1, 1, and 10?µM) of deltamethrin in the primary hepatocyte culture of Lake Van fish were investigated via liver enzymes aspartase aminotransferase (AST) and alanine aminotransferase (ALT), and the total antioxidant status (TAS), total oxidant status (TOS), lipid peroxidation (MDA), and DNA damage (8-OHdG).

Deltamethrin caused an increase in the AST and ALT levels dependent on the dosage and time. The TAS and TOS levels increased at the end of 24?h and there was no difference at the end of 48?h. Deltamethrin did not affect the MDA level, but increased the 8-OHdG (P?<?0.05). In conclusion, it can be said that high doses of deltamethrin (1 and 10?µM) have a toxic effect on the primary hepatocyte culture of Lake Van fish.     

Protective effects of Flacourtia indica on doxorubicin-induced cardiotoxicity in rats

This study examined the cardioprotective activity of an ethanolic extract of Flacourtia indica (FI) against doxorubicin (DOX)-induced myocardial infarction (MI) in rats. Different phytoconstituents were identified by gas chromatography-mass spectroscopy. DOX is a chemotherapeutic agent which produces free oxygen radicals that result in serious dose-limiting cardiotoxicity. A DOX dose of 20?mg?kg^?1 body weight is used to bring significant changes in biochemical parameters, endogenous antioxidants, and moderate necrosis in the heart. The pretreatment with FI at two doses (250 and 500?mg?kg^?1) to DOX-treated rats significantly prevented the altered biochemical parameters such as serum marker enzymes serum glutamate-pyruvate transaminase, serum glutamate oxaloacetate transaminase, creatine phosphokinase, and lactate dehydrogenase, lipid profile such as low-density lipoprotein, very low-density lipoprotein, triglycerides, high-density lipoprotein, total cholesterol, and antioxidant parameters such as superoxide dismutase, glutathione, catalase, glutathione peroxidase, and malondialdehyde to near normal level. Serum urea, uric acid, and alkaline phosphate which are increased on DOX administration registered near normal values on pretreatment with FI. In conclusion, these data suggest that the ethanol extract of FI can prevent heart damage by DOX-induced MI in rats and this is likely mediated through its antioxidant activities.     

DNA damage in mouse organs and in human sperm cells by bisphenol A

Abstract

The in vivo genotoxic potential of bisphenol A using the comet assay in mice and in human sperm cells in vitro without metabolizing enzymes was studied. Male mice were exposed by oral gavage to the following doses of bisphenol A (0 125, 250 and 500?mg/kg body weight). DNA damage was investigated in liver, kidney, testes, urinary bladder, colon and lungs cells. In testicular cells, a significant increase in DNA strand breaks was observed in the lowest, but not in the medium or highest dose groups. Histopathological investigation of the testicular samples did not show any treatment dose-related effects. No DNA strand breaks were observed in any of the other investigated tissues. In human sperm cells in vitro, bisphenol A did not induce DNA strand breaks.     

Toxicological studies of zinc oxide nanomaterials in rats

In this study, we have evaluated the ability of zinc oxide (ZnO) nanoparticles to induce pulmonary and extrapulmonary toxicities was examined in rats following intratracheal (IT) instillation. Lungs of rats were instilled IT with either phosphate-buffered saline (PBS)?+?1% Tween 80, ZnO nanoparticles, carbonyl iron or quartz particles at a dose of 1 or 5?mg?kg^?1 body weight. Following exposure, bronchoalveolar lavage (BAL) fluid, blood samples and organs including lung, liver, kidneys, heart, pancreas, and brain were collected at 24?h, 1 week, or 1 month of post instillation of nanoparticles and different parameters estimated to assess toxicity. BAL fluid was analyzed for lactate dehydrogenase (LDH) and alkaline phosphatase (ALP) to assess pulmonary toxicity. Exposures to ZnO or quartz particles produced transient dose-dependant increase in BAL fluid LDH and ALP activities at all post exposure periods. Blood samples were analyzed for the tissue damage biomarkers to assess extrapulmonary toxicity. Histopathological examination of lung, liver and kidneys revealed dose-dependent degeneration and necrosis which worsened at 1 week post-instillation periods but recovered at 1 month post instillation. Histopathological examination of rat pancreas, heart, and brain exposed to quartz or ZnO particles showed no marked changes. Data suggest the instillation of ZnO nanoparticles produced a greater pulmonary toxicity in rats comparable with quartz; and extrapulmonary toxicities of these ZnO nanoparticles might be due to translocation into liver and kidney.