Administration Of Lead Acetate Research Articles

Metabolic Effect of Acute Lead and Restraint Stress Exposure on Female Wistar Rats

Lead is a common environmental toxicant while restraint stress is primarily a psychological stressor. Lead exposure and psychological stressors, are known to exert adverse effects on metabolic health independently. The aim of this study is to investigate the metabolic effects of acute lead and restraint stress exposure in female Wistar rats. Twenty-four (24) female Wistar rats weighing 180 - 240 grams were randomly divided into four (4) groups (n=6): Control (CTL), Restraint stress alone (RSA), Lead acetate alone (LDA), Restraint stress + Lead acetate (RSL). The duration of the study was 21 days. The lead acetate alone group were orally administered 100mg/kg of lead acetate, the restraint stress alone group were restrained for 1 hour daily and the restraint stress + lead group were administered lead acetate and restrained for 1 hour daily. Twenty-four hours post last lead administration and restraint stress exposure, all animals were anesthetized and sacrificed. Blood was collected via cardiac puncture for biochemical analysis. Results showed serum low-density lipoprotein (LDL), triglycerides (TAG) and total cholesterol (CHO) levels in lead alone and restraint stress alone groups were significantly increased (p<0.05) compared with control. The restraint + lead group showed a significant increase in serum LDL, TAG and CHO levels when compared with control, lead alone and restraint stress alone groups. Serum HDL levels showed no significant difference across all groups. Serum glucose, insulin and cortisol levels in lead alone and restraint stress alone groups were significantly increased (p<0.05) when compared with control. The restraint + lead group showed a significant increase (p<0.05) in serum glucose, insulin and cortisol levels when compared with control, lead alone and restraint alone groups. In conclusion, this study showed that exposure to restraint stress and lead has a significant effect on the metabolic profile of female Wistar rats.

Biotin Supplementation Improved Reproductive Parameters Following Lead Induced Testicular Toxicity in Male Wistar Rats

Lead acetate, a prominent heavy metal, is released into the environment by various industries like paint, ceramics, lead-containing pipes, and plastics. Exposure to lead acetate has adverse effects on numerous organs in the body, with a particular impact on the testes due to its distinctive vascular system. The present study investigated the potential protective effects of biotin on lead acetate-induced testicular damage in Wistar rats. Twenty (20) male Wistar rats were divided into 4 groups: control (animal feed daily with water); negative control (lead acetate 60 mg/kg); Positive control group( high-dose Biotin (80mg/kg) and the treatment group Lead acetate (60mg/kg)/high-dose Biotin (80mg/kg). After 28 days of administration, blood samples were collected for hormonal assay, and semen from the epididymis for semen profile. Testicular samples were also collected for histopathological studies. Results showed that lead acetate administration significantly decreased the sperm count, motility, viability, and altered histology of the testis (testicular damage, necrosis of seminiferous tubules, and loss of spermatid) compared to the negative control. However, the treatment group showed significantly improved histology of the testis, and increased sperm count, motility, and viability. From the results of this study, it could be concluded that biotin supplementation could provide a promising ameliorative effect against lead acetate-induced testicular toxicity.

Alchornea laxiflora (Benth.) Pax & K. Hoffman extract protects against lead-induced neurodegeneration in cockerel chickens

Lead (Pb) is a ubiquitous, non-biodegradable heavy metal contaminant with a significant impact on both human and animal health. The adverse effect of lead on health and productivity of avian species has received little attention. Alchornea laxiflora (Benth) belongs to Euphorbiaceae family and grows naturally in the Nigerian rain forest. Decoction of the leaves is usually administered traditionally to treat inflammatory and infectious diseases. The ethanol extract of Alchornea laxiflora (EaAL) leaves was used in this study to ameliorate lead-induced neurodegeneration.Seven groups of 5-week-old cockerels (n=5) were treated for 6 weeks thus: Group A - Control (water only), Group B - (100 mg/kg of EaAL daily), Group C - (200 mg/kg of EaAL daily, p.o.), Group D - (1 % lead acetate in drinking water), Group E - (1 % lead acetate in drinking water and 100 mg/kg of EaAL daily), Group F - (1 % lead acetate and 200 mg/kg of EaAL daily), Group G - (1 % lead acetate and 100 mg/kg of Vitamin C). All administrations were per os birds were euthanized on day 43 by quick cervical dislocation. Histological stains (H&E and Nissl) and Black Gold II (BGII) histochemistry were used to assess alterations in the cerebrum and cerebellum.Administration of EaAL at the two concentrations resulted in a drastic reduction in the incidence of neuropathologies observed (e.g. pyknosis and multilayering of Purkinje cells, neuronal degeneration in hippocampus cerebrum and ependymal cells, distortion of meningeal epithelial cells, etc). BGII histochemistry revealed severe demyelination caused by the administration of lead acetate, while the two doses of EaAL showed significant restoration of myelin in the cerebellum. The amelioration of demyelination observed with the use of vitamin C was considerably lower than that recorded with the use of EaAL.The use of EaAL significantly ameliorated morphological alterations and demyelination caused by the administration of lead acetate, however, caution should be exercised in the administration, as individual species idiosyncrasies may arise and the tendency to pro-oxidation at 200 mg/kg when administered alone was observed in one subject.

Chronic Lead Exposure Impairment of Hypothalamic-Pituitary-Gonadal Axis in Adult Male Wistar Rats: Biochemical and Histomorphological Evidence

Introduction: The upsurge in male infertility has been associated with impaired hypothalamic-pituitary-gonadal (HPG) axis. There is a dearth of conclusive empirical data as to the deleterious impacts of heavy metal intoxication on male reproductive functioning through the HPG axis. Objective: This study seeks to elucidate the possible effects of chronic lead exposure on HPG signalling activities via biochemical and histopathological assessment. Experimental Section/Material and Methods: Forty adult male Wistar rats were randomised into four experimental groups (n=10). Group A, the control group received standard feed and water ad libitume. In Groups B, C and D, animals were orally administered lead acetate at concentrations of 2.5% 3.0% and 3.5%, respectively, using a stock solution of 150mg/kg once daily for 35 days. After the treatment period, all animals were fasted overnight and euthanized by cervical dislocation. Blood levels of anterior pituitary hormones (FSH and LH) were analysed using standard methods. Statistical analyses was done on graph pad prism. Testicular tissue was processed routinely for histopathological analyses using different stains. Results: Hormonal assays showed no significant changes in follicle-stimulating hormone (FSH) and luteinizing hormone (LH) (p>0.05) levels across groups. However, histological examination revealed alterations in testicular architecture, including disrupted spermatogonia cell arrangement and reduced Sertoli cell numbers, indicative of adverse effects on spermatogenesis. Conclusion: Chronic lead exposure adversely affects testicular histomorphology in adult male Wistar rats, potentially impacting reproductive function. While hormonal levels remain relatively unaffected, alterations in testicular structure suggest a direct impact on gonadal functions at a cellular level.

Ethanol extract of galangal (Alpinia Galanga) administration on degeneration, necrosis, and inflammatory cells in the proximal tubules of male mice (Mus musculus) exposed to lead acetate

Introduction: This study aimed to investigate the preventive effect of the ethanolic extract of galangal (Alpinia galanga) on degeneration, necrosis, and inflammatory cells in the kidney proximal tubules of male mice (Mus musculus) exposed to lead acetate. Objective: This was a pure experimental laboratory study using a completely randomized approach/randomized posttest only control group design. Twenty-five male mice (Mus musculus) were divided into five treatment groups: negative control (K-) received 0.5% CMC Na and aquades, positive control (K+) received induction of 20 mg/kgBW lead acetate for 20 days, and P1, P2, and P3 groups received oral administration of galangal ethanol extract from day 1 to day 24 as preventive measures with successive doses of (P1) 200 mg/kgBW, (P2) 400 mg/kgBW, and (P3) 800 mg/kgBW, respectively. Lead acetate administration at a dose of 20 mg/kgBW started from day 4 to day 24. On the 25th day, all groups were sacrificed, and kidney tissues were harvested for histopathological examination using the scoring method. Histopathological data analysis was performed using the Kruskal-Wallis test followed by Mann-Whitney U test to compare differences between groups. Results: The Mann-Whitney U test showed a significant increase in degeneration, necrosis, and infiltration of inflammatory cells in the kidney proximal tubules of male mice (Mus musculus) exposed to lead acetate (p < 0.05). Administration of galangal ethanol extract significantly reduced degeneration, necrosis, and infiltration of inflammatory cells (p < 0.05). The highest dose of galangal ethanol extract (800 mg/kg BW) exhibited a significant decrease in degeneration, necrosis, and infiltration of inflammatory cells (p < 0.05), comparable to the normal condition (K-). Conclusion: Administration of ethanol extract of galangal (Alpinia galanga) effectively prevented lead acetate-induced degeneration, necrosis, and infiltration of inflammatory cells in the kidney proximal tubules of male mice (Mus musculus).

Protective effect of 1, 8-cineole (eucalyptol) against lead-induced liver injury by ameliorating oxidative stress and inflammation and modulating TLR4/MyD88/NF-κB signaling.

This study was conducted to explore the impact of 1, 8-cineole (eucalyptol) on the biochemical, molecular, and histological changes caused by lead acetate in the liver of adult male Wistar rats. The research also investigated the potential involvement of the TLR4 signaling pathway in this effect. Rats were orally administered lead acetate (25 mg/kg-day) for 14 consecutive days and received 1, 8-cineole (100 mg/kg-day) during the same period. 1, 8-cineole prevented an increase in the malondialdehyde level, a decrease in the glutathione level, and a decrease in the activity of superoxide dismutase and glutathione peroxidase enzymes in the liver of rats treated with lead acetate. This monoterpene also prevented an increase in the expression of pro-inflammatory cytokines and significantly reduced the infiltration of inflammatory cells in the liver parenchyma. Additionally, 1, 8-cineole discouraged the increase in toll-like receptor 4 (TLR4), myeloid differentiation primary response 88 (MyD88), and nuclear factor kappa B (NF-κB) expression in the liver and stopped a rise in serum AST and ALT enzymes. 1, 8-cineole can prevent liver damage caused by lead acetate by reducing oxidative stress and inflammation. This hepatoprotection is probably achieved by inhibiting TLR4/MyD88/NF-κB signaling.

Antagonistic effectiveness of Anacardium occidentale leaf extract on lead-acetate exposure-induced hepatorenal toxicity in rats.

Lead (Pb) poisoning is an environmental substance that accumulates in the hepato-renal tissue, which is hazardous to health, while Anacardium occidentale L. is a tropical herb used to treat oxidative stress and inflammatory diseases. The aim of this study was to investigate the antagonistic effect of Anacardium occidentale leaf extract on lead acetate exposure-induced hepatorenal toxicity in rats. Thirty-six adult Wistar rats were split into six equal groups (n = 6). Group I served as a control, and groups II and III were administered lead acetate (50 mg/kg) and Anacardium occidentale leaf extract (400 mg/kg), respectively, while rats in groups IV-VI were administered Anacardium occidentale (L) extract (200 mg/kg and 400 mg/kg) and 10 mg/kg of Succimer, respectively, and were then administered lead acetate (50 mg/kg). When compared to the group I, rats administered lead acetate showed an increase in hepatic enzymes, urea, creatinine, MDA, TNF-α, and IL-1β (p < 0.001) levels and decreased levels of SOD, CAT, and GSH, whereas Anacardium occidentale prevented the increase in hepatorenal function parameters, oxidative stress, and inflammatory markers (TNF-α and IL-1β) induced by lead acetate. Rats administered only lead acetate had a marked increase in hepatic Pb concentration, severe hepatic steatosis, and renal glomerulus degeneration. However, treatment with Anacardium occidentale extract and succimer decreases the Pb concentration, oxidative stress, and inflammation, and also reduces histological liver steatosis and glomerular cytoarchitecture deterioration in the kidney. The results of this study revealed that Anacardium occidentale extract protects against lead acetate-induced liver and kidney toxicity by decreasing oxidative stress and inflammation.

Protective Role of Myricetin and Fisetin Against Nephrotoxicity Caused by Lead Acetate Exposure through Up-regulation of Nrf2/HO-1 Signalling Pathway.

The effect of various flavonoids against oxidative stress and inflammation caused by lead exposure has been investigated. However, the protective effects of myricetin (MYC) and fisetin (FST), which are known to have potent antioxidant properties, against nephrotoxicity caused by exposure to lead acetate (LA), the water-soluble form of lead, have not been investigated. Our study investigated the protective role of these flavonoids against LA intoxication-induced nephrotoxicity. In our study, 42 male rats were used. The rats were randomly selected and divided into 6 groups. These groups were: control, LA (100g/kg), LA + MYC (100mg/kg), LA + MYC (200mg/kg), LA + FST (100mg/kg) and LA + FST (200mg/kg). All chemicals were administered daily by gavage for 28 days. According to the experimental protocol, the animals were sacrificed and their kidney tissues were isolated. Serum biochemical parameters, histological examinations, levels of several trace elements, oxidative stress and inflammatory parameters at both biochemical and molecular levels in kidney tissues were examined. After LA administration, tissue lead levels increased and zinc levels decreased. This situation was reversed by MYC and FST treatment. Oxidative stress and inflammatory response were increased in the kidney tissue of LA-treated rats and renal function was impaired. It was observed that both doses of MYC and high dose of FST could prevent nephrotoxicity. Oral administration of both doses of MYC and high dose FST ameliorated the changes in biochemical, oxidative and inflammatory parameters. Restoration of normal renal tissue architecture was also demonstrated by histological studies. MYC and FST were found to have promising biological activity against LA-induced nephrotoxicity, acting by attenuating inflammation and oxidative stress and improving antioxidant status.

Effects of fabomatisol under lead intoxication in rat experiment

The conducted study indicates the priority use of the drug fabomatizole to protect living systems from the negative effects of lead acetate.Aim: To study the mechanisms of fabomatizole effect on the nature of changes in redox reactions, NO-forming function of the endothelium, cholesterol metabolism and functional parameters in rats with lead intoxication.Material and Methods. The study was carried out on 60 Wistar rats. Lead intoxication was induced by intramuscular administration of lead acetate at a dose of 5 mg/kg of animal weight for a month. At the end of the intoxication period, Fabomatizol was administered at a dose of 10 mg/kg for a month. Next, blood and tissue samples were taken from rats to determine the activity of oxidative, antioxidant, enzymatic systems, nitric oxide metabolism, and blood lipid spectrum.Results. The data obtained showed that intramuscular administration of fabomatisol in case of lead intoxication has an antioxidant effect and inhibits lipid peroxidation (LPO) activity. Under the influence of fabomatizol, nitric oxide metabolism andtotal nitric oxide metabolites (NOx) content significantly increased, and a negative correlation was found between the malondialdehyde level, superoxide dismutase activity and NOx. At the same time, the study found a decrease in the expression level of eNOS as the cause of a reduced concentration of NOx in the blood. L-arginine availability for eNOS was disturbed by atherogenic low density lipoprotein (LDL). Treatment with fabomatizol against the background of lead intoxication caused a decrease in total cholesterol, LDL cholesterol and an increase inhigh density lipoprotein cholesterol. By inhibiting lipid peroxidation in the cells of the renal and hepatic tissues, fabomatizol contributed to the restoration of lipid-protein interactions and the functional activity of Na and K-activated ATPase in the renal interstitium. Simultaneously, there is an activation of Na,K-ATP-ase in the hepatocyte and a decrease in the level of organ-specific enzymes in the blood plasma.Conclusion. The results obtained are evidence of the antioxidant properties of fabomatisol in lead intoxication, its ability to induce the activity of antioxidant system (AOS enzymes, stimulate the NO-forming function of the endothelium, NOx production and the activity of the membrane enzyme – Na,K-ATP-ase in the renal and hepatic tissues and reduce the level of organ-specific enzymes in blood plasma.

Naphthaleneoxypropargyl-Containing Piperazine as a Regulator of Effector Immune Cell Populations upon an Aseptic Inflammation.

This study investigated the effects of aseptic inflammation and heavy metal exposure on immune responses, as well as the potential immunomodulatory properties of the newly synthesized 1-[1-(2,5-dimethoxyphenyl)-4-(naphthalene-1-yloxy)but-2-ynyl]-4-methylpiperazine complexed with β-cyclodextrin (β-CD). Aseptic inflammation was induced by a subcutaneous injection of turpentine in rats, while heavy metal exposure was achieved through a daily administration of cadmium chloride and lead acetate. The levels of immune cell populations, including cytotoxic T lymphocytes (CTL), monocytes, and granulocytes, were assessed in the spleen. The results showed that aseptic inflammation led to decreased levels of CTL, monocytes, and granulocytes on the 14th day, indicating an inflammatory response accompanied by a migration of effector cells to the inflamed tissues. The exposure to cadmium chloride and lead acetate resulted in systemic immunotoxic effects, with reduced levels of B cells, CD4+ Th cells, monocytes, and granulocytes in the spleen. Notably, piperazine complexed with β-CD (the complex) exhibited significant stimulatory effects on CD4+, CD8+, and myeloid cell populations during aseptic inflammation, even in the presence of heavy metal exposure. These findings suggest the potential immunomodulatory properties of the complex in the context of aseptic inflammation and heavy metal exposure.

Mollification of Lead Induced Liver Injury by Lycopersicon esculentum (Tomato) Extract

Objective: Lead is a highly toxic, non-biodegradable heavy metal usually found in the environment largely as a pollutant of water, soil or air. Chronic lead exposure has adverse effects on human health. Lycopersicon esculentum has many phytochemicals that may ameliorate organ injury due to lead toxicity in humans. This study answered the question “Is aqueous extract of Lycopersicon esculentum (tomato) beneficent to lead toxicity induced liver injury?”&#x0D; Methodology: The study had five groups with fifteen animals each. The control was group CN. The lead toxicity group (PbT) had 30 mg/kg/day of lead acetate crystals, the concomitant extract group (CE) had concurrent administration of lead acetate and aqueous extract of L. esculentum (at 400 mg/kg). The post lead toxicity low dose extract. (PLE) had sequential administration of lead acetate and aq. extract L. esculentum (at 400 mg/kg). The post lead toxicity high dose extract. (PHE) had sequential administration of lead acetate and aq. extract L. esculentum (at 800 mg/kg). Both the lead acetate and extract were administered orally for twenty one days. At specific periods, blood samples were collected for biochemical analyses and organs harvested for histopathological evaluation.&#x0D; Result: The total plasma protein levels of the extract groups (CE, PLE and PHE) were significantly higher than that of the PbT group. The PbT group had markedly elevated plasma liver enzymes. Oxidative stress was only evident in the PbT group but not in the extract groups as suggested by the significantly depressed anti-oxidant activities and elevated lipid peroxidation. A cystic lesion was observed in one of the liver specimens from the PbT group. Histopathological findings included fatty infiltration of the liver in the PbT group and presence of multinucleated hepatocytes in the extract groups. The latter feature suggested the ability of aqueous extract of L. esculentum to ameliorate the lead (Pb) toxicity induced liver damage.&#x0D; Conclusion: Concurrent and post-exposure administration of aqueous extract of tomato fruit (L. esculentum) mollified the liver injury caused by lead toxicity.

Sub‑chronic administration of lead alters markers of oxidative stress, acetylcholinesterase and Na+K+‑ATPase activities in rat brain.

This study investigated the effects of sub‑chronic administration of lead (Pb) acetate on thiobarbituric acid reactive substances (TBA‑RS), total sulfhydryl content, protein carbonyl content, antioxidant enzymes (superoxide dismutase [SOD], catalase [CAT], glutathione peroxidase [GSH‑Px]), acetylcholinesterase (AChE), and Na+K+‑ATPase in the cerebral structures of rats. Male Wistar rats aged 60 days were treated with saline (control group) or Pb (treatment group), at various doses, by gavage, once a day for 35 days. The animals were sacrificed twelve hours after the last administration, and the cerebellum, hippocampus and cerebral cortex were removed. The results showed that Pb did not alter the evaluated oxidative stress parameters. Furthermore, Pb (64 and/or 128 mg/kg) altered SOD in the cerebellum, cerebral cortex and hippocampus. Pb (128 mg/kg) altered CAT in the cerebellum and cerebral cortex and GSH‑Px in the cerebral cortex. Also, Pb (64 mg/kg and 128 mg/kg) altered GSH‑Px in the cerebellum. Moreover, Pb (128 mg/kg) increased AChE in the hippocampus and decreased Na+K+‑ATPase in the cerebellum and hippocampus. In conclusion, sub‑chronic exposure to Pb (occupational and environmental intoxication) altered antioxidant enzymes, AChE, and Na+K+‑ATPase, contributing to cerebral dysfunction.

Effects of sinapic acid on lead acetate-induced oxidative stress, apoptosis and inflammation in testicular tissue.

In this study, the effect of lead acetate (PbAc) and sinapic acid (SNP) administration on oxidative stress, apoptosis, inflammation, sperm quality and histopathology in testicular tissue of rats was tried to be determined. PbAc was administered at a dose of 30 mg/kg/bw for 7 days to induce testicular toxicity in rats. Oral doses of 5 and 10 mg/kg/bw SNP were administered to rats for 7 days after PbAc administration. According to our findings, while PbAc administration increased MDA content in rats, it decreased GPx, SOD, CAT activity and GSH content. NF-kB, IL-1β, TNF-α, and COX-2, which are among the inflammation parameters that increased due to PbAc, decreased with the administration of SNP. Nrf2, HO-1, and NQO1 mRNA transcript levels decreased with PbAc, but SNP treatments increased these mRNA levels in a dose-dependent manner. RAGE and NLRP3 gene expression were upregulated in PbAc treated rats. MAPK14, MAPK15, and JNK relative mRNA levels decreased with SNP treatment in PbAc treated rats. While the levels of apoptosis markers Bax, Caspase-3, and Apaf-1 increased in rats treated with PbAc, the level of Bcl-2 decreased, but SNP inhibited this apoptosis markers. PbAc caused histopathological deterioration in testis tissue and negatively affected spermatogenesis. When the sperm quality was examined, the decrease in sperm motility and spermatozoon density caused by PbAc, and the increase in the ratio of dead and abnormal spermatozoa were inhibited by SNP. As a result, while PbAc increased apoptosis and inflammation by inducing oxidative stress in testicles, SNP treatment inhibited these changes and increased sperm quality.

Clinical haematobiochemical parameters during experimental lead poisoning in goats: effects of methanol extract of Tiger nuts

The effects of methanol extract of tiger nut on haematobiochemical parameters during experimental lead poisoning in Red Sokoto goats were investigated. The seeds of tiger nuts were extracted with 90% methanol. Phytochemical analyses were carried out using standard procedures. A total of twenty-four adult Red Sokoto goats of both sexes were separated randomly into four groups for acute and chronic studies. Three goats in both acute and chronic studies were housed per group. In the acute and chronic studies DW groups was administered an equivalent amount of distilled water (400 and 200 ml/kg). Group II was only administered lead acetate (400 and 200 mg/kg). Group III was administered with methanol extract of tiger nuts (400 and 200 mg/kg) combined with lead acetate (400 and 200 mg/kg) respectively. Group IV was administered with tiger nuts (400 and 200 mg/kg) only for a period of 2 and then 20 weeks for acute and chronic phases respectively. Haematobiochemical parameters were determined. The lead acetate and lead acetate combined with methanol extract of tiger nut in acute and chronic groups showed microcytic normocytic and microcytic hypochromic anaemia respectively with the latter suggestive that with chronicity, an enzymatic inhibition of haemoglobin synthesis led to iron deficiency. Alterations in serum biochemical enzymes and other parameters indicative of hepato-renal injury were observed and ameliorated by methanol extract from tiger nuts

The effects of aqueous extract of ocimum gratissimum on the cerebellum of male wistar rats challenged by lead acetate

•Chronic lead acetate toxicity was induced in male rats by oral administration.•Effect of Ocimum gratissimum in lead acetate toxicity on the cerebellum.•Oral lead acetate administration led to oxidative stress in the cerebellum.•Ocimum gratissimum extract attenuated oxidative stress and enhanced antioxidant enzymes.•Ocimum gratissimum ameliorated lead acetate-induced toxicity in the cerebellum. ObjectivesLead acetate (LA) is a known toxicant, and its exposure in the environment has been on the increase in recent times, leading to oxidative stress and tissue damage. Based on this background, we investigated the role of the antioxidative properties of Ocimum gratissimum (OG), a potent medicinal plant, in ameliorating and protecting the brain from lead acetate-induced cerebellar damage via the assessment of oxidative stress parameters and brain histology.MethodsThirty-five adult male Wistar rats weighing 145–200g divided into five groups were used for this experimental study. Groups 1, 2, and 3 served as positive and negative controls and were administered sterile water, 252.98 mg/kg body weight of aqueous leaves extract of OG and 120 mg/kg of LA for 21 days. Furthermore, following the administration of LA, rats in groups 4 and 5 were treated with 125 and 250 mg/kg body weight of OG. OG and LA were administered orally for 42 days. Oxidative stress parameters, as well as histoarchitectural investigations following LA and OG treatment, were analysed.ResultsResults showed normal histoarchitecture of the cerebellum in control and group 2 animals (OG only). In group 3 animals that received LA only, we observed severe stages of neurodegenerative features in the Purkinje, granular cell molecular cell layers of the Cerebellum. Also, results from groups 4 and 5 rats that were co-administered with LA and OG revealed regenerative tendencies and an increase in the neuronal cell density of the cerebellum. Nevertheless, we recorded an increase in the brain content of malondialdehyde and decreased antioxidant status (catalase (CAT), glutathione (GSH), and sodium dismutase (SOD)) following LA administration. OG attenuated this heightened MDA activity and depletion of the antioxidant status.ConclusionOverall, these findings suggest that oral administration of aqueous extract of OG improved cerebellar neurotoxicity and degeneration in rats exposed to LA by modulating oxidative damage. Lead acetate (LA) is a known toxicant, and its exposure in the environment has been on the increase in recent times, leading to oxidative stress and tissue damage. Based on this background, we investigated the role of the antioxidative properties of Ocimum gratissimum (OG), a potent medicinal plant, in ameliorating and protecting the brain from lead acetate-induced cerebellar damage via the assessment of oxidative stress parameters and brain histology. Thirty-five adult male Wistar rats weighing 145–200g divided into five groups were used for this experimental study. Groups 1, 2, and 3 served as positive and negative controls and were administered sterile water, 252.98 mg/kg body weight of aqueous leaves extract of OG and 120 mg/kg of LA for 21 days. Furthermore, following the administration of LA, rats in groups 4 and 5 were treated with 125 and 250 mg/kg body weight of OG. OG and LA were administered orally for 42 days. Oxidative stress parameters, as well as histoarchitectural investigations following LA and OG treatment, were analysed. Results showed normal histoarchitecture of the cerebellum in control and group 2 animals (OG only). In group 3 animals that received LA only, we observed severe stages of neurodegenerative features in the Purkinje, granular cell molecular cell layers of the Cerebellum. Also, results from groups 4 and 5 rats that were co-administered with LA and OG revealed regenerative tendencies and an increase in the neuronal cell density of the cerebellum. Nevertheless, we recorded an increase in the brain content of malondialdehyde and decreased antioxidant status (catalase (CAT), glutathione (GSH), and sodium dismutase (SOD)) following LA administration. OG attenuated this heightened MDA activity and depletion of the antioxidant status. Overall, these findings suggest that oral administration of aqueous extract of OG improved cerebellar neurotoxicity and degeneration in rats exposed to LA by modulating oxidative damage.

Analysis of the Mechanisms of Impairment of Functional Parameters of Internal Organs in Saturnism in an Experiment in Rats

In rats with lead intoxication (intramuscular administration of lead acetate in a dose 5 mg/kg for 30 days), the development of oxidative stress, reduced expression of endothelial NO synthase and total metabolites of NO production, as well as an increased content of norepinephrine were observed. Lead-induced nephropathy developed; diuresis and sodium excretion increased due to a decrease in tubular transport of water and sodium ions. Activation of free-radical reactions in cells of the renal cortex and medulla contributed to inhibition of Na,K-ATPase. LPO caused damage to cardiomyocytes, hepatocytes, which was seen from elevation of AST, ALT, γ-glutamyl transpeptidase, and alkaline phosphatase in the blood serum and a decrease in activity of Na,K-ATPase in the organs tissues. Metabolic disorders revealed in saturnism in experimental rats (LPO activation, reduced expression of endothelial NO synthase and total metabolites of NO, and increased blood norepinephrine) contributed to the development of vascular endothelial dysfunction and hemodynamics disturbances, and damage to cells of internal organs: kidney, myocardium, liver.

HISTOPATHOLOGY OF RAT KIDNEY EXPOSED TO LEAD HEAVY METAL

Lead is a non-essential heavy metal which is toxic to kidney, carcinogenic, and teratogenic if get inside animal or even human’s body. The research aims to determine the histopatologic view of rat’s kidney which was exposed to lead with different doses. The research uses 20 of 2 months old Wistar strain white rat with 250-300 g body weight. The research uses completely randomized design with 4 treatments, which is control (P0), 0.5 ppm lead acetate (P1), 1.0 ppm lead acetate (P2), and 2.0 lead acetate (P3). Treatment were given daily for 30 days and on day 31 euthanation and necropsy was performed then the kidney tissue was removed and put into 10% neutral buffer formalin. Then histopathologic preparation with hematoxilyn eosin stain was made. Kidney histopathology changes that were examined were bleeding, necrosis, and inflammation. Severity of the lesion was made into scoring wiith mild category of it was focal, moderate if it was multifocal, and severy if it was diffuse. The Kruskal-Wallis test of the histopathologic examination result of rat’s kidney which was exposed to lead acetate shows a significant bleeding, necrosis and even nephritis (inflammation) lesion compared to without the exposure to lead acetate (control). The Mann-Whitney test shows a significant result which varies between bleeding, necrosis, even nephritis (inflammation) lesion. with a It can be concluded that the administration of lead acetate with the dose of 0.5 ppm, 1.0 ppm, even 2.0 ppm can cause bleeding, necrosis even nephritis compared to control and the administration of 2.0 ppm dose shows the most severe lesions. There needs to be a continued research regarding the effects of lead with higher doses.

Amino acid balance of microbial-tissue complex in the small intestinal and liver under administration of lead acetate

It is known that the initiating event of liver damage during lead intoxication is the effect of lead on the intestinal microbiome and the metabolic profile of enterocytes. The aim of the study was to reveal the dependence of the concentrations of free amino acids and their derivatives in the liver on the amino acid pool of the microbial-tissue complex of the small intestine. We used rats weighing 120‒140 g, which were injected intragastrically for three weeks with drinking water with lead acetate. Free amino acids and their nitrogen-containing metabolites in the microbial-tissue complex of the intestine and liver were determined by HPLC. Enteral intake of lead acetate with drinking water changes the profile of free amino acids and their derivatives in the microbial-tissue complex of the small intestine, which correlates with a violation of amino acid homeostasis in the liver. The analysis of the correlations of the indicators we determined indicates the essential role of nitrogen-containing metabolites of amino acids ‒ ethanolamine and phosphoethanolamine, taurine, and cystathionine. The direction of the correlation relationship between various nitrogen-containing metabolites of the microbial-tissue complex and the liver can be considered as marker of discoordination of homeostasis.

Aqueous Hypoestes rosea Leaf extract Ameliorates Lead-Acetate-Induced Thyroid Hormones Disruption in Albino Wistar Rats

Aim: To evaluate the effect of aqueous extract of Hypoestes rosea (AEHR) leaf extract on thyroid hormones in lead-acetate-induced Albino Rats.&#x0D; Study design: Experimental study.&#x0D; Place and Duration of Study: Department of Pharmacology, University of Port Harcourt and Department of Chemical Pathology, University of Port Harcourt, between October, 2019 and March, 2020.&#x0D; Methodology: A total of 140 albino Wistar rats were used for the study. The animals were divided into 26 groups (6 post-treatment and 6 pre-treatment groups for female rats and the same number for male rats). Each group contained 5 rats for both sexes in both pre- and post-treatments groups, except the positive control groups that had 10 animals for both sexes. The study was carried out for 21 days in each sex. The negative control groups received rat feed only, the extract control (EC) group received 100mg/kg bwt/day for 21 days, the positive control (PC) group received 60mg/kg b.wt per day of lead acetate for 7 days. The other 3 groups received 100mgkg, 200mg/kg and 300mg/kg b.wt respectively for 14 days either as pre-treatment or post treatment, for both sexes of the albino rats. At the end of the experimental periods, the rats were sacrificed under chloroform anaesthesia and samples were taken through the jugular vein. Thyroid hormone levels (thyroid stimulating hormone (TSH), tri-iodothyronine (T3) and tetra-iodothyronine (T4)) were estimated using the Enzyme linked immunosorbent assay methods. Statistical analysis was done using Statistical Analysis System (SAS), STAT 15.1 and p values less than 0.05 were considered statistically significant.&#x0D; Results: The results showed that the administration of lead acetate in male and female rats caused significant (p&lt;0.05) fall in the levels of TSH, fT3 and fT4. The plant in a dose dependent pattern was able to significantly (p&lt;0.05), reverse the effect of lead acetate in the post treatment phase and also protect the endocrine system from the deleterious effect of lead acetate in the pre-treatment phase.&#x0D; Conclusion: This study shows that the consumption of AEHR by albino rats could help protect the endocrine system against endocrine disruptors.

МОРФОФУНКЦИОНАЛЬНОЕ СОСТОЯНИЕ РЕПРОДУКТИВНОЙ СИСТЕМЫ БЕЛЫХ КРЫС В НОРМЕ И ПРИ ВОЗДЕЙСТВИИ СВИНЦА

Lead, being a widespread environmental pollutant, affects both the male and female reproductive systems of humans and experimental animals. However, many issues remain unclear, including the morphofunctional state of the placenta and gonads in lead intoxication, which leads to various disorders in the development of the fetus and newborn. It follows from the foregoing that this issue requires a comprehensive and comprehensive study. In the present work, the morphological parameters of the placenta and ovaries of female rats were established after 7 days of oral exposure to lead acetate at a dose of 45 mg/kg of body weight. It was shown that after exposure to lead acetate, morphofunctional restructuring of the cortical and medulla of the ovary of nulliparous female white rats was observed. The cells of the single-layer epithelium covering the ovary from the outside acquire an elongated shape. The protein shell is compacted. There is an increase in the volume of the medulla of the ovary in relation to the cortical, due to the enlargement of the vessels, which indicates an increase in the blood supply to the ovary. In the cortical substance of the ovary, primordial follicles are located mainly singly. Among the more mature forms of follicles, follicles of oval and irregular shape were identified. The yellow bodies found have an irregular shape. In pregnant animals treated with lead acetate, attention is drawn to the high content of atretic follicles. The administration of lead acetate to pregnant rats causes pronounced ultrastructural changes in the labyrinthine zone of the placenta, expressed by thinning of the cyto- and syncytiotrophoblast, vacuolization and clarification of the cytoplasmic matrix, destruction of mitochondria, and a decrease in intercellular contacts between cyto- and syncytiotrophoblastic elements. Against the background of edema and destruction of the trophoblastic structures of the labyrinthine zone of the placenta, the presence of areas with numerous osmiophilic formations was noted. These changes in the placenta can be considered specific for lead intoxication.