Sodium Arsenite Group Research Articles

Protective and antidote effect of Foeniculum vulgare against Sodium Arsenite induced hepatotoxicity and testicular toxicity in Charles Foster rats

Arsenic poisoning in groundwater is the most common environmental pollutant, which is leading to serious pollution worldwide. Chronic arsenic exposure from drinking water to humans causes major public health-related issues. The present study was conducted to investigate the antidote effects of Foeniculum vulgare (Fennel) against arsenic-induced hepatotoxicity and testicular toxicity in Charles Foster rats. In the present study, twenty-four male Charles Foster rats (120±5gm) were divided into four Groups (n=6), where control Group-I received a normal diet and water; Group - II and Group - III received sodium arsenite (8 mg per kg body weight per day) for 90 days. Group III was left with a normal diet and water for the next 60 days for auto-recovery. The group IV rats were administered Foeniculum vulgare (Funnel) hydroxyl ethanolic seed extract at a dose of 150 mg per kg body weight for 60 days in a 90-day pre-treated sodium arsenite group (8 mg per kg body weight). After complete dose duration, all the treated animals were sacrificed the same day for haematological, biochemical, hormonal, and histopathological studies. In the arsenic treated rats, there were significant (p<0.001) changes in serum levels of SGPT, SGOT, urea, uric acid and creatinine as well as in haematological parameters. And there was also decease in the sperm count and sperm motility, accompanied by an increased incidence of sperm abnormalities and hormonal imbalances leading to infertility. In contrast, after the administration of F. vulgare seeds hydroxy-ethanolic extract to arsenic-treated rats, significant (p<0.001) improvements were observed in hepatic and renal parameters as well as haematological parameters. In the arsenic-intoxicant rat, after administration of F. vulgare seeds hydroxyl ethanolic extract, there was a significant (p<001) reduction in the arsenic concentration in blood, liver, and kidney tissues as well as serum LPO. The histopathological study also showed the F. vulgare seeds hydroxy-ethanolic extract significantly restored the cellular integrity of testicular cells, leading to their normal functioning against arsenic-induced toxicity.

Effects of zingerone on rat induced testicular toxicity by sodium arsenite via oxidative stress, endoplasmic reticulum stress, inflammation, apoptosis, and autophagy pathways.

This study aimed to investigate the effects of zingerone (ZNG) treatment on testicular toxicity in rats induced by sodium arsenite (SA). In the study, five groups were formed (n=7) and the experimental groups were designated as follows; Vehicle group, ZNG group, SA group, SA+ZNG 25 group, and SA+ZNG 50 group. While SA was administered orally to rats at 10 mg/kg/bw, ZNG was given to rats orally at 25 and 50 mg/kg/bw doses for 14 days. As a result of the presented study, an increase was observed in the MDA contents of the testicular tissue of the rats administered SA, while significant decreases were observed in GSH levels, SOD, CAT, and GPx activities. The mRNA transcript levels of the pro-inflammatory genes NF-κB, TNF-α, IL-1β, and IL-6 were triggered after SA administration. Additionally, SA administration caused inflammation by increasing RAGE, NLRP3, and JAK-2/STAT3 gene expression. Moreover, endoplasmic reticulum (ER) stress occurred in the testicular tissues of SA-treated rats and thus ATF-6, PERK, IRE1, and GRP78 genes were up-regulated. SA caused apoptosis by up-regulating Bax and Caspase-3 expressions and inhibiting Bcl-2 expression in testicles. SA caused histological irregularities in the testicles, resulting in decreased sperm quality. ZNG treatment reduced SA-induced oxidative stress, ER stress, inflammation, apoptosis, and histological irregularities in the testicles while increasing sperm quality. As a result, it was observed that ZNG could alleviate the toxicity caused by SA in the testicles.

The Effects of Vitamin C on the Quality of Semen, Testicular Tissue, and Apoptosis in Mice Exposed to Sodium Arsenite

Background: Arsenic is a heavy metal that causes malformation. It affects the reproductive system of men by induction of oxidative stress.
 Objectives: This study investigated the effect of Vitamin C (Vit C), as a potent antioxidant, on sperm quality and testicular tissue in mice that received sodium arsenite.
 Methods: A total of 28 adult male NMRI mice were divided into four groups: control, sodium arsenite (7 mg/kg/d), Vitamin C (Vit C; 150 mg/kg/d), and sodium arsenite+Vit C (with previous doses). Gavage treatments were administered for 35 days. At the end of the treatments, the right testis was used for histopathological observations and apoptosis assessment, and the left testis to evaluate sperm parameters.
 Results: Sperm parameters such as count, motility, viability, morphology, tail length, Daily Sperm Production (DSP), the diameter of seminiferous tubules, the height of the germinal epithelium, and the number of germ cells and Sertoli cells were significantly decreased in the sodium arsenite group compared to the control group (P<0.05). Malondialdehyde levels were significantly increased, and serum testosterone levels were significantly reduced in the sodium arsenite group. The mentioned parameters were compensated for in the sodium arsenite+Vit C group compared to the sodium arsenite group (P<0.05).
 Conclusion: Vitamin C can decrease the undesired changes induced by sodium arsenite in the male reproductive system.

Chrysin attenuates sodium arsenite-induced nephrotoxicity in rats by suppressing oxidative stress and inflammation

BackgroundWe aimed to study the beneficial property of chrysin (CHR) by targeting its antioxidant and anti-inflammatory effects on nephrotoxicity induced by sodium arsenite (SA). Materials & methodsWe have used the 35 male Wistar rats in five equal groups (n = 7). Normal saline in (5 ml/kg; p.o.; 21 days) was given to the control group. Sodium arsenite (10 mg/kg; p.o.; 14 days) was given to the SA group. CHR (25, 50 and 100 mg/kg; p.o.; 21 days) and SA (10 mg/kg; p.o.; 14 days from the 7th day of the experiment) was given to the SA + CHR 25, 50 and 100 groups. On the 22nd day of the experiment, the animals’ bloods and kidneys were taken, and then we have performed functional, biochemical and histological assessment. ResultsCHR pre- and alongside administration (more potently at dose of 100 mg/kg) with SA reduced the SA-induced alterations in serum creatinine and blood urine nitrogen levels. Increased levels of protein carbonyl, myeloperoxidase, malondialdehyde and nitric oxide in kidney tissue were decreased by CHR treatment. CHR administration increased the levels of glutathione and activities of glutathione peroxidase, catalase and superoxide dismutase in renal tissue. Moreover, treatment with CHR reduced the levels of inflammatory mediators including interleukin 1 beta and tumor necrosis factor alpha in renal tissue. The renal histological lesions induced SA were mitigated by CHR treatment in dose dependent manner. ConclusionThe results of present study suggested that administration of CHR before and alongside with SA attenuated the renal toxic effects of SA via antioxidative stress and anti-inflammatory effects.

Polyphenol‐rich fraction ofAlchornea cordifolialeaf ameliorates arsenite‐induced infertility in male rats

Alchornea cordifolia is used traditionally for the treatment of infertility and venereal diseases. Thirty rats were randomly divided into five groups of six rats each: Group 1 (distilled water), group 2 (7 mg/kg sodium arsenite), group 3 (7 mg/kg sodium arsenite and 100 µg/kg polyphenol-rich fraction 1 of A. cordifolia), group 4 (7 mg/kg sodium arsenite + 100 µg/kg polyphenol-rich fraction 2) and group 5 (7 mg/kg sodium arsenite + α-tocopherol). The experiment lasted 30 consecutive days. Biochemical markers of oxidative stress and antioxidants, male reproductive hormones, spermatozoa function tests, histopathology, immunoreactivity of androgen receptor binding protein (ARBP) and anti-apoptotic B-cell lymphoma-2 protein expressions were estimated. Data were analysed using descriptive statistics and ANOVA at p < .05. Treatment with AF1 significantly decreased markers of oxidative stress, but increased the systemic antioxidants, testosterone, FSH, spermatozoa count and motility. Histopathological lesions of necrosis and germinal epithelial sloughing observed in sodium arsenite group were absent in sodium arsenite + 100 µg/kg polyphenol-rich fraction 1 group. Expressions of androgen receptor binding protein and anti-apoptotic B-cell lymphoma-2 were highest in sodium arsenite + 100 µg/kg polyphenol-rich fraction 1 group. In conclusion, the polyphenol-rich fraction of A. cordifolia is protective against sodium arsenite-induced infertility in male rats through the inhibition of oxidative and apoptotic mechanisms.

Reproductive disorders in female rats after prenatal exposure to sodium arsenite

Arsenic is a metalloid widely found in the environment in organic and inorganic forms. Exposure to inorganic arsenic forms via drinking water has been associated with an increased incidence of negative health effects, including reproductive disorders and dysfunction of the endocrine system. However, the impact of arsenic exposure on female reproductive development is still unclear. Therefore, in the present study, we evaluated the effects of prenatal exposure to arsenic on the initial sexual development and puberty onset, and in the morphology of the female reproductive organs, estrous cycle regularity and fertility parameters during adulthood. To do that, pregnant female Wistar rats were exposed to 10mg/L sodium arsenite via drinking water from gestational day (GD) 1 until GD 21 and the female offspring was evaluated in different postnatal days. Our results showed that prenatal arsenic exposure induced a decrease of litter weight and morphological masculinization in females at postnatal day 1. Moreover, these females had a delay in the age of puberty onset and alteration in estrous cycle number and length. During adulthood, females from the sodium arsenite group showed an increase in endometrium, myometrium and perimetrium areas, and an imbalance in uterine antioxidant enzyme activity. These animals also presented an increase in post-implantation loss and reabsorption number, leading to reduced viable fetus number. In conclusion, prenatal arsenic exposure in rats was able to promote female masculinization, alter sexual development and impair reproductive performance.

The effects of hesperidin on sodium arsenite-induced different organ toxicity in rats on metabolic enzymes as antidiabetic and anticholinergics potentials: A biochemical approach.

In our work, it was purposed to investigate the effects of sodium arsenite (SA) and hesperidin (HSP) administered to rats on some metabolic enzymes including carbonic anhydrase (CA), aldose reductase (AR), paraoxonase-1 (PON1), α-glycosidase (α-Gly), butyrylcholine esterase (BChE), acetylcholine esterase (AChE) enzymes activities in the brain, heart, liver, testis, and kidney tissues of rats. CA activities were significantly decreased in testis, liver, and heart tissues of rats given HSP, SA, SA+HSP-100, and SA+HSP-200 compared to control (p<0.05). In liver tissue, AChE and BChE enzymes activities were significantly reduced given in all groups. In all tissues, α-Gly activity was reduced given in all groups. In the current study, aldose reductase enzyme activity was reduced significantly in testis, brain, and heart tissues of all groups compared to standard (p<0.05). PON1 enzyme activity was increased significantly in kidney and liver tissues of rats HSP groups and decreased SA groups compared to control. PRACTICAL APPLICATIONS: α-Glycosidase is the key enzyme involved in the digestion of the carbohydrate. Another enzyme α-amylase hydrolyzes the α-linked polysaccharide derivatives into oligosaccharide molecules, and α-glycosidase enzymes, which are characterized in small intestine, catalyze the final stage in the digestive mechanism of carbohydrate molecule to release absorbable monosaccharides like glucose. Conforming to the cholinergic hypothesis, impairment of the cholinergic pathways plays a good role in the development of neurodegenerative diseases like depression, schizophrenia, Alzheimer's disease (AD) problems with the regulation of traumatic brain injury and sleep. The AD is the main reason for dementia disease, and mild to moderate cases are generally treated with AChE inhibitors. Human CA inhibitor compounds are clinically used for more than 70 years as antiglaucoma and diuretics drugs.

Spirulina platensisameliorates arsenic-mediated uterine damage and ovarian steroidogenic disorder

Novel, non-invasive, painless oral therapeutic agents are needed to replace the painful conventional treatment of arsenic-associated health hazards with metal chelators. Our aim was to examine the effect of spirulina ( Spirulina platensis ( Geitler, 1925 )) on arsenic-mediated uterine toxicity. Female Wistar rats were divided equally into four experimental treatment groups: control group, sodium arsenite group (1.0 mg/100 g body mass), spirulina placebo group (20 mg/100 g body mass), and sodium arsenite + spirulina group. In contrast with the control group, spectrophotometric and electrozymographic evaluation revealed that rats that ingested arsenic for 8 d showed significant diminution of the activities of superoxide dismutase, catalase, and peroxidase ( p &lt; 0.001). Mutagenic uterine DNA breakage and tissue damage were prominent following arsenic consumption by the rats. Oral delivery of spirulina resulted in a significant amelioration of arsenic-induced adverse oxidative stress and genotoxic state of rats. A significant low-signaling ( p &lt; 0.001) of gonadotropins and estradiol was also noted in the arsenic-treated rats, which was terminated by spirulina; this arsenic-primed adverse effect was significant ( p &lt; 0.05, p &lt; 0.01). The spirulina treatment mechanism could be associated with augmentation of the antioxidant defense system that protects the arsenic-mediated pathological state of the uterus.

Methanol Extract of Adansonia digitata Leaf Protects Against Sodium Arsenite-induced Toxicities in Male Wistar Rats.

Background:Human and animal population exposure to arsenic through the consumption of arsenic contaminated water is rampant in many parts of the world. Protective agents of medicinal plants origin could provide maximum protection against toxicities of various kinds.Objective:The protective role of orally administered methanol extract of the leaves of Adansonia digitata (MELAD) on sodium arsenite (SA) – induced clastogenicity and hepatotoxicity in male Wistar rats was evaluated.Materials and Methods:Thirty male Wistar rats divided into six Groups (1–6) of five animals each were used for the study. Group 1 (negative control) received distilled water and normal diet only, Groups 2–6 received the extract (at 250 or 500 mg/kg body weight) and/or SA at 2.5 mg/kg body weight.Results:There was statistically significant (P < 0.05) increase in the number of micronucleated polychromatic erythrocytes and lipid peroxidation in the SA group as compared with the negative control and treated groups. Administration of the extract reduced the effects of SA on the above parameters. Activities of serum alanine and aspartate aminotransferases did not show statistically significant effects; however, the histological analyses revealed periportal cellular infiltration by mononuclear cells, whereas the MELAD treated groups show mild cellular infiltration and mild portal congestion.Conclusions:MELAD protect against SA-induced toxicities in rats, and it may offer protection in circumstances of co-exposure and cases of arsenicosis.SUMMARY MELAD extract significantly reduce the lipid peroxidation induced by sodium arsenite in the liver of rats.MELAD did not show profound effects on the activities of serum alanine (ALT) and aspartate (AST) aminotranferases.MELAD offered significant protection against sodium arsenite-induced genotoxicity in the micronuclei induction assay.In the circumstances of co-exposure to arsenic contamination, MELAD may protect against sodium arsenite-induced toxicities. Abbreviations Used: MELAD: Methanol extract of the leaves of Adansonia digitata, SA: Sodium arsenite, nMPCEs: Number of micronucleated polychromatic erythocytes; ALT: Alanine aminotranferase; AST: Aspartate aminotranferase, TBARS: Thiobarbituric acid reactive substances, TBA: Thiobarbituric acid, MDA: malondialdehyde, Sodium arsenite (NaAsO2), IARC: International Agency for Research on Cancer

Effect of curcumin on kidney histopathological changes, lipid peroxidation and total antioxidant capacity of serum in sodium arsenite-treated mice

Sodium arsenite is an environmental pollutant with the ability to generate free radicals and curcumin acts as a potent antioxidant. This study investigates the effect of curcumin on kidney histopathology, lipid peroxidation and antioxidant capacity of serum in the mice treated with sodium arsenite. Adult male mice were divided into four groups: control, sodium arsenite, curcumin and curcumin+sodium arsenite. The treatments were delivered for 5 weeks. After the treatment period, blood samples were collected and the concentrations of malondialdehyde (MDA) and total antioxidant capacity of serum were determined. Left kidney was dissected, weighed and used for histopathological and histomorphometrical studies. Sodium arsenite-treated mice showed a significant decrease in the diameter of glomerulus and proximal tubule, glomerular area, total antioxidant capacity of serum as well as a significant increase in serum concentration of MDA compared to the control group. However, no significant difference was found in kidney weight, area and diameter of Bowman's capsule as well as the diameter of distal tubule in mice treated with sodium arsenite compared to the control. In curcumin+sodium arsenite group, curcumin significantly reversed the adverse effects of sodium arsenite on the diameter of glomerulus and proximal tubule, glomerular area, total antioxidant capacity of serum and serum concentration of MDA compared to the sodium arsenite group. The application of curcumin alone significantly increased the total antioxidant capacity of serum compared to the control. Curcumin compensated the adverse effects of sodium arsenite on kidney tissue, lipid peroxidation and total antioxidant capacity of serum.

Curcumin Inhibits The Adverse Effects of Sodium Arsenite in Mouse Epididymal Sperm.

The aim of this study was to investigate the effects of curcumin on epididy- mal sperm parameters in adult male Navel Medical Research Institute (NMRI) mice ex- posed to sodium arsenite. In this experimental study, we divided the animals into four groups: control, sodium arsenite (5 mg/kg), curcumin (100 mg/kg) and curcumin+sodium arsenite. Exposures were performed by intraperitoneal injections for a 5-week period. After the exposure period, we recorded the animals' body and left testes weights. The left caudal epididymis was used to count the sperm number and analyze motility, viability, morphological abnormalities, acrosome reaction, DNA integrity, and histone-protamine replacement in the spermatozoa. One-way analysis of variance (ANOVA) followed by the Tukey's test was used to assess the statistical significance of the data with SPSS 16.0. P<0.05 was considered significant. Mice exposed to sodium arsenite showed a significant decrease in the num- ber, motility, viability, normal sperm morphology and acrosome integrity of spermato- zoa compared to the control group. In the curcumin+sodium arsenite group, curcumin significantly reversed these adverse effects to the point where they approximated the control. In addition, the application of curcumin alone had no significant difference in these parameters compared to the control and curcumin+sodium arsenite groups. However, we observed no significant differences in the body and the testis weight as well as the DNA integrity and histone-protamine replacement in the spermatozoa of the four groups. Curcumin compensated for the toxic effects of sodium arsenite on a number of sperm parameters in adult mice.

Protective effect of silymarin on viability, motility and mitochondrial membrane potential of ram sperm treated with sodium arsenite

Sodium arsenite can impair male reproductive function by inducing oxidative stress. Silymarin is known as a potent antioxidant. This study was performed to investigate if silymarin can prevent the adverse effect of sodium arsenite on ram sperm viability, motility and mitochondrial membrane potential. Epidydimal spermatozoa obtained from ram were divided into five groups: 1) Spermatozoa at 0 hr, 2) spermatozoa at 180 min (control), 3) spermatozoa treated with sodium arsenite (10 μM) for 180 min, 4) spermatozoa treated with silymarin (20 μM) + sodium arsenite (10 μM) for 180 min and 5) spermatozoa treated with silymarin (20 μM) for 180 min. MTT assay and Rhodamine 123 staining were used to assess sperm viability and mitochondrial membrane potential respectively. Sperm motility was performed according to World Health Organization (WHO) guidelines. Viability (p<0.01), nonprogressive motility (p<0.001) and intact mitochondrial membrane potential (p<0.001) of the spermatozoa were significantly decreased in sodium arsenite treated group compared to control group. In silymarin + sodium arsenite group, silymarin could significantly reverse the adverse effect of sodium arsenite on these sperm parameters compared to sodium arsenite group (p<0.001). In addition, the application of silymarin alone for 180 minutes could significantly increase progressively motile sperm (p<0.001) and decrease non motile sperm (p<0.01) compared to the control. Silymarin could compensate the adverse effect of sodium arsenite on viability, nonprogressive motility and mitochondrial membrane potential of ram sperm.

Silymarin protects plasma membrane and acrosome integrity in sperm treated with sodium arsenite

Exposure to arsenic is associated with impairment of male reproductive function by inducing oxidative stress. Silymarin with an antioxidant property scavenges free radicals. The aim of this study was to investigate if silymarin can prevent the adverse effects of sodium arsenite on ram sperm plasma membrane and acrosome integrity. Ram epidydimal spermatozoa were divided into five groups: spermatozoa at 0 hr, spermatozoa at 180 min (control), spermatozoa treated with silymarin (20 μM) + sodium arsenite (10 μM) for 180 min, spermatozoa treated with sodium arsenite (10 μM) for 180 min and spermatozoa treated with silymarin (20 μM) for 180 min. Double staining of Hoechst and propidium iodide was performed to evaluate sperm plasma membrane integrity, whereas comassie brilliant blue staining was used to assess acrosome integrity. Plasma membrane (p< 0.001) and acrosome integrity (p< 0.05) of the spermatozoa were significantly reduced in sodium arsenite group compared to the control. In silymarin + sodium arsenite group, silymarin was able to significantly (p< 0.001) ameliorate the adverse effects of sodium arsenite on these sperm parameters compared to sodium arsenite group. The incubation of sperm for 180 min (control group) showed a significant (p< 0.001) decrease in acrosome integrity compared to the spermatozoa at 0 hour. The application of silymarin alone for 180 min could also significantly (p< 0.05) increase sperm acrosome integrity compared to the control. Silymarin as a potent antioxidant could compensate the adverse effects of sodium arsenite on the ram sperm plasma membrane and acrosome integrity.

A Comparative Study of the Effects of Sodium Arsenite and Nanoparticles of Sodium Arsenite on the Apparent and Skeletal Malformations in Rat Embryos

BACKGROUND AND OBJECTIVE: Arsenic causes congenital anomalies in humans and animals, and nanoparticles of sodium arsenite are highly capable of inducing apoptosis. Since the effects of nanoparticles of sodium arsenite on fetal malformations have not been evaluated yet, this study aims to compare the effect of sodium arsenite and nanoparticles of sodium arsenite on skeletal malformations in rat embryos. METHODS: This in-vitro study was performed on four groups of pregnant rats (n= 23 rats). Mating was confirmed by observation of vaginal plug. On the tenth day of gestation, pregnant rats in different groups received intraperitoneal normal saline (n=7 rats), sodium arsenite (11 mg/kg) (n=5 rats), nanoparticles of sodium arsenite (1 mg) (n=5 rats) and nanoparticles of sodium arsenite (11 mg) (n=7 rats). All the rats were euthanized on the twentieth day of pregnancy and their embryos were removed, their weight and length were measured, and then were stained with alizarin red and alcian blue. The skeletal system abnormities of embryos such as cleft palate, malfunctions or malformations in ribs, vertebrae, spine, sternum, arms, legs, fingers and reduction of ossification were evaluated by a stereomicroscope, and then compared with the control group. FINDINGS: Sodium arsenite and nanoparticles of sodium arsenite reduced fetal weight from 5 g in the control group to 2 g (p≤0.033) and also, decreased fetal length from 38 cm to 28 cm in the control group (p≤0.023). The weight and length of fetuses were significantly reduced in nanoparticles of sodium arsenite group (11 mg), as compared to sodium arsenite group (p≤0.033). There were no skeletal malformations in the control group, while the percentage of anomalities was between 3% and 47% in the intervention group. CONCLUSION: Nanoparticles of sodium arsenite, as compared to sodium arsenite, were more effective in reducing fetal length and weight and in diminishing the rate of skeletal malformations such as cleft palate.

Arsenic induced histological alterations in testis of Swiss albino mice and protection by Chlorophytum borivilianum

To investigate the sodium arsenite induced damages on the reproductive system of male mice as well as to examine whether Chlorophytum borivilianum ( C. borivilianum ) is able to ameliorate the damages. A different group of adult Swiss albino mice was made such as control group, sodium arsenite group, post combination group, pre and post combination group. After the treatment, the testis was removed, weighed and processed for histopathological observation. Cauda epididymis was used to observe abnormal sperms. A highly significant depletion was found in all the germ cell populations such as spermatogonia A and B, primary and secondary spermatocytes, spermatids in arsenic treated group with respect to control whereas recovery is found in combination groups. The results conclude that C. borivilianum significantly protects against arsenic-induced damages.

Histological and histometrical study of the protective role of α-tocopherol against sodium arsenite toxicity in rat ovaries.

This study examines histometrical changes induced by sodium arsenite (SA), as an environmental pollutant, and investigates the protective effect of α-tocopherol on ovaries of SA-treated rats during the prenatal stage until sexual maturity. Rats were classified into groups: control, SA (8 ppm/day), α-tocopherol (100 ppm/day), and SA+α-tocopherol. Treatment was performed from pregnancy until maturation when the rats and ovaries were weighed. The Cavalieri method was used to estimate volume of the ovaries, cortex, medulla, and corpus luteum. The mean diameter of oocytes, granulosa cells, and nuclei were measured and volume was estimated using the Nucleator method. The number of oocytes and thickness of the zona pellucida (ZP) were determined using an optical dissector and orthogonal intercept method, respectively. SA reduced the body and ovary weight, the number of secondary, antral and Graafian oocytes, volume of the ovaries, cortex, medulla and corpus luteum, mean diameter and volume of oocytes in primordial and primary follicles, mean diameter and volume of oocyte nuclei in all types of follicles, and mean thickness of the ZP in secondary and antral follicles. Also, the mean diameter and volume of granulosa cells and their nuclei in antral and Graafian follicles decreased significantly. Vacuolization and vascular congestion in the corpus luteum and an increase in the number of atretic oocytes were seen in the SA group. Most of these parameters were unchanged from the control level in the SA+α-tocopherol group. It was concluded that α-tocopherol supplementation reduced the toxic effects of SA exposure on ovarian tissue in rats.

Amelioration by chlorophytum borivilianum upon arsenic induced oxidative stress in Swiss albino mice

Background: Arsenic, a major water pollutant in India, produces toxic effects on male reproductive system due to oxidative stress. Arsenic contaminated drinking water causes several health problems such as Blackfoot disease, hypertension, diabetes mellitus, disturbances in the nervous system and cancers of liver, kidney, lung and bladder in humans. Aim: This study accessed the efficacy of Chlorophytum borivilianum in reducing arsenic-induced biochemical and nucleic acid damages in mice testis. Methods: A different group of adult Swiss albino mice was made such as control group, C. borivilianum group, sodium arsenite group and combination group. For antioxidant activity, ABTS radical cation decolorization assay was done. Body and testis weight, protein, sialic acid, ATPase activity, DNA and RNA content in the testis were also estimated. Results: Animals exposed to sodium arsenite at the dose of 4.0 mg/kg b.wt. showed significant decrease (p&lt;0.001) in testicular protein, sialic acid, ATPase activity, DNA and RNA content indicate DNA damage and apoptosis whereas combination group showed a significant increase in all the parameters. Conclusion: The results thus led us to conclude that administration of C. borivilianum at the dose of 800 mg/kg b.wt. Significantly protects against arsenic-induced oxidative stress. Keywords: ABTS Assay; Atpase; DNA; Oxidative Stress; Protein; Sialic Acid.

Effect of vitamin E on sperm number and testis histopathology of sodium arsenite-treated rats

The aims of this study were to investigate the adverse effects of sodium arsenite on the reproductive system of male rats as well as to examine whether vitamin E is able to ameliorate these effects. Adult rats were divided into four groups: 1/ control, 2/ sodium arsenite (8 mg/kg/day), 3/ vitamin E (100 mg/kg/day), and 4/ sodium arsenite +vitamin E group. Treatments were administered orally by gavage for eight weeks. After treatment, body and left testis weights were recorded and the testis was used for the histological analysis. Left cauda epididymis was used to count sperm number. Body and testis weight did not differ among the groups (p>0.05). A significant decrease (p<0.001) in sperm number and mean diameter of seminiferous tubules as well as a significant increase (p<0.001) in the mean diameter of seminiferous tubules' lumen were found in sodium arsenite group compared to those of controls. Sodium arsenite did not affect the morphology and diameter of spermatogonial nucleus (p>0.05). In the sodium arsenite + vitamin E group, vitamin E ameliorated (p<0.001) the adverse effects of sodium arsenite on sperm number as well as the diameters of tubule and lumen. In addition, the treatment of rats with vitamin E alone significantly (p<0.001) increased the diameter of seminiferous tubules and significantly (p<0.001) decreased seminiferous tubules' lumen compared to the control group. Vitamin E appeared to ameliorate the adverse effects of sodium arsenite on epididymal sperm number and some morphometrical parameters of the adult rat testis.

Model establishment of liver fibrosis in oral arsenic solution exposed mice

To discuss and compare the model establishment of liver fibrosis in oral arsenic solution exposed mice and mice with high-fat feedstuff. A total of 240 mice were divided randomly into 6 groups: control group, sodium arsenite group, sodium arsenate group, high-fat feedstuff group, sodium arsenite group with high-fat feedstuff and sodium arsenate group with high-fat feedstuff with 40 mice each. Control group and high-fat feedstuff group (drinking tap water), sodium arsenite group and sodium arsenite group with high-fat feedstuff (drinking 300 mg/L iAs3+ water), sodium arsenate group and sodium arsenate group with high-fat feedstuff (drinking 300 mg/L iAs5+ water). The mice were sacrificed after 3, 6, 10 months' arsenic-exposure and examined for liver function. HE dyeing and Masson dyeing were also employed to observe the pathological changes in hepatic tissue in each group. After 3 months' modeling, ALT and AST in control group, sodium arsenite group, sodium arsenate group, sodium arsenite group with high-fat feedstuff and sodium arsenate group with high-fat feedstuff were (36.7 +/- 5.7) U/L and (110 +/- 22) U/L, (55.6 +/- 4.6) U/L and (249 +/- 41) U/L, (52.6 +/- 8.8) U/L and (161 +/- 15) U/L, (311.3 +/- 19.7) U/L and (484 +/- 15) U/L and (515.0 +/- 60.8) U/L and (671 +/- 24) U/L. They were higher in all the arsenic groups than in control group (P < 0.05); all the HE dyeing samples in arsenic groups showed liver injury in varying degrees such as hydropic degeneration, fatty degeneration, spotty necrosis, focal necrosis and inflammatory cell infiltration. There were liver cell regeneration and fibroplasia in varying degrees. The liver injury of the mice in all arsenic groups aggravated as exposure time prolonged. Masson dyeing after 10 months' modeling showed hyperplasia in portal areas and central venous areas; the mean area of fibrosis in control group, sodium arsenite group, sodium arsenate group, sodium arsenite group with high-fat feedstuff and sodium arsenate group with high-fat feedstuff were 0.1333, 0.5584, 0.5250, 0.7534 and 0.7200 respectively. There was statistical significance between arsenic groups and control group (P < 0.05) The liver injury and fibrosis model in oral arsenic solution exposed mice and those with high-fat feedstuff are successfully established and subsequently evaluated. It is a comparatively ideal animal model for studying arsenic liver injury and fibrosis.