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The current research was constructed to throw the light on the protective possibility of Chlorella vulgaris ( C. vulgaris ) and Spirulina platensis ( S. platensis ) against lead acetate-promoted testicular dysfunction in male rats. Forty rats were classified into four groups: (i) control, (ii) rats received lead acetate (30 mg/kg bw), (iii) rats concomitantly received lead acetate and C. vulgaris (300 mg/kg bw), (vi) rats were simultaneously treated with lead acetate and S. platensis (300 mg/kg bw) via oral gavage for 8 weeks. Lead acetate promoted testicular injury as expressed with fall in reproductive organ weights and gonadosomatic index (GSI). Lead acetate disrupted spermatogenesis as indicated by sperm cell count reduction and increased sperm malformation percentage. Lead acetate-deteriorated steroidogenesis is evoked by minimized serum testosterone along with maximized follicle-stimulating hormone (FSH) and luteinizing hormone (LH) levels. Testicular oxidative, inflammatory, and apoptotic cascades are revealed by elevated acid phosphatase (ACP) and sorbitol dehydrogenase (SDH) serum leakage, declined testicular total antioxidative capacity (TAC) with elevated total oxidative capacity (TOC), tumor necrosis factor alpha (TNF-α), caspase-3 levels, lessened androgen receptor (AR) expression, and histopathological lesions against control. Our research highlights that C. vulgaris or S. platensis therapy can modulate lead acetate-promoted testicular dysfunction via their antioxidant activity as expressed by elevated TAC and reduced TOC, immunomodulatory effect as indicated by lessened TNF-α level, and anti-apoptotic potential that was revealed by minimized caspase-3 levels. As well as restoration of testicular histoarchitecture, androgen receptor, steroidogenesis, and spermatogenesis were detected with better impacts to S. platensis comparing with C. vulgaris . Therefore, further clinical trials are needed to test S. platensis and C. vulgaris as a promising candidate in treating male infertility.

In this study, the protective effects of chrysin (CR) on lead acetate (PbAc)-induced renal toxicity in Sprague-Dawley rats were investigated with biochemical, histopathological, and immunohistochemical methods. In the study, rats were given orally at 30 mg/kg/body weight (BW) PbAc after CR of 25 and 50 mg/kg/BW was administered to them orally (a total of 7 administrations for 7 days). The results showed that CR reduced urea and creatinine levels by alleviating PbAc-induced kidney damage. It was determined that CR decreases PbAc-induced lipid peroxidation due to its antioxidant properties and increases catalase (CAT), superoxide dismutase (SOD), glutathione peroxidase (GPx) activities, and glutathione (GSH) levels. It was also detected that CR protects DNA from the toxic effects of PbAc and reduces 8-hydroxy-2′-deoxyguanosine (8-OHdG) levels. Biochemical and immunohistochemical findings demonstrated that CR had anti-inflammatory and antiapoptotic effects and reduced nuclear factor kappa-B (NF-κB), interleukin-33 (IL-33), prostaglandin-E2 (PGE-2), tumor necrosis factor-α (TNF-α), p53 levels, and the activities of cyclooxygenase-2 (COX-2) and inducible nitric oxide synthase (iNOS), which were increased with PbAc administration. Moreover, CR was found to increase the levels of aquaporin-1 (AQP-1) and nephrine in PbAc-induced kidney tissue. CR decreased the contents of lead (Pb), zinc (Zn), iron (Fe), sodium (Na), and copper (Cu) and increased those of potassium (K) calcium (Ca) in renal tissue. These results indicated that CR considerably alleviates kidney toxicity caused by PbAc.

Lead (Pb) is one of the most common heavy metals with toxicological effects on many tissues in humans as well as animals. In order to counteract the toxic effects of this metal, the administration of synthetic or natural antioxidants is thus required. The aim of this study was to examine the beneficial effect of the aqueous extract of Ononis natrix (AEON) against lead acetate-induced damage from a behavioral, biochemical, and histological point of view. Forty-eight male mice were divided into four equal groups: Ctr (control); Pb (lead acetate 1g/l); Pb + On 100 mg/kg (lead acetate 1 g/l + AEON 100 mg/kg); Pb + On 500 mg/kg (lead acetate 1 g/l + AEON 500 mg/kg). AEON was administered orally from day 21 after the start of lead exposure up to the end of the experiment. The results revealed that lead induced behavioral disorders, increased serum levels of liver markers (AST, ALT, and bilirubin), as well as kidney markers (urea and creatinine). At the same time, levels of thiobarbituric acid reactive substances (TBARS) and glutathione peroxidase (GPx) increased significantly. Moreover, Pb caused structural changes in the liver and kidneys of Pb-exposed mice. However, AEON administration significantly improved all lead-induced brain, liver, and kidney dysfunctions. Our results suggest that AEON could be a source of molecules with therapeutic potential against brain, liver, and kidney abnormalities caused by lead exposure.

Lead (Pb) poisoning is one of the pivotal environmental issues and prompts liver dysfunction by elevating oxidative stress and inflammation. Nicotinamide (NA) deficiency enhances sensitivity to Pb toxicity. So, we investigated the effect of nicotinamide (NA) on the rat’s liver histopathological and biochemical profiles in a rat model of Pb toxicity. Thirty-six rats were divided into four groups (nine rats at each): normal (N), lead toxicity (Pbt), and NA-treated N and Pbt groups. Treated groups took NA (180 mg/L in drinking water for one month). Pb intoxication was motivated in rats by acquiring 50 mg/L lead acetate in drinking water. Oxidative stress markers (advanced oxidation protein products and malondialdehyde), antioxidant markers (total glutathione, reduced glutathione to oxidized glutathione ratio, ferric ion reducing power, catalase, and paraoxonase-1), and inflammatory markers (hepatic nuclear factor-kβ expression, interleukin 1β level, and myeloperoxidase activity) in sera and liver homogenates were determined. In addition, the biochemical parameters of the liver function were measured. Finally, the liver of rats was evaluated by histopathological observation. NA corrected lead-persuaded biochemical and histopathological changes in the rat’s liver. In addition, treatment decreased Pb, oxidative stress, and inflammatory markers in the sera and liver homogenates of N and Pbt groups. In addition, it elevated antioxidant markers (p < 0.001). NA prevented Pb-induced liver histopathological alternations and reduced liver dysfunction by reducing Pb, oxidative stress, and inflammation. Moreover, raising GSH/GSSG and diminishing the hepatic NF-kβ pathway are cardinal mechanisms of the treatment against Pb-motivated hepatotoxicity in rats.

Exposure to environmental pollutants tightly impacts on the male fertility. In the present study, we examined the toxic effects of lead acetate (Pb) on testicular structure and the possible effect of quercetin on mitigating these effects. The apoptotic changes in the testes were also studied by the TUNEL assay and changes in apoptosis-related gene (Bax, Bcl-2, and caspase-3) expression. Twenty-one male mice were randomly divided into 3 groups of control, Pb, and lead acetate + quercetin. Testicular weight, both absolute and relative, was higher in Pb-exposed mice in comparison with the control and Pb-quercetin groups. The increase in size of testis was related to the lumen and connective tissue in this group. Lead acetate induced different patterns in testicular cell number; as spermatogonia, spermatocyte, and Sertoli cells number did not affect in lead acetate exposed group, while total number of round spermatids and long spermatids significantly reduced. In addition, Bcl-2 expression was downregulated, and Bax expression was upregulated in Pb-treated group in comparison with the control and Pb + quercetin groups. The TUNEL assay revealed that the number of apoptotic cells in Pb-treated group were increaed significantley in comparison to other groups. In conclusion, Pb administration adversely impacted on the cellular organization and activation of the apoptotic pathways in the testis; on the other hand, quercetin co-administration with lead partially ameliorated these adverse effects.

Environmental pollutant effects on fertility sometime are irretrievable. The aim of this study was to investigate the effect of lead acetate and quercetin on tight (claudin 11 and occludin) and gap junctional (connexin 43) proteins and the integrity of the blood–testis barrier status. Experimental groups, including the lead acetate (Pb), quercetin (QE), lead acetate with quercetin (Pb + QE), and control mice, were treated at least one spermatogenic cycle. Gene expression of claudin 11 and occludin decreased in Pb + QE, Pb, and QE compared with the control group. Connexin 43 (Cx43) expression in the control and Pb groups was lower than in Pb + QE and QE. The immunohistochemical data were generally in line with these findings. In conclusion, the results showed that Pb exposure led to disorders in cellular interactions that affect testicular function; however, simultaneous treatment with quercetin did not alleviate these effects.

This study was designed to determine the lead or cadmium exposure of Barki rams and the beneficial role of Nannochlorposis oculata ( N. oculata ) 4% as a feed supplement, as well as its mitigating role against these elements’ impacts concerning performance, biochemical markers of liver enzymes and kidney function, thyroid hormone activity, and oxidative stress markers. Six groups of 36 Barki rams (33.63 ± 1.29 kg) were divided into G1: which served as control; G2: was given 4% dietary N. oculata ; G3: was given oral 1 mg/kg cadmium chloride; G4: was given 5 mg/kg/day lead acetate; G5: was given oral 1 mg/kg cadmium chloride and 4% dietary N. oculata , and G6: was given oral 5 mg/kg/day lead acetate and 4% dietary N. oculata ; and treatments were continued for 60 days. Cadmium and lead-exposed groups exhibited lower and weaker weight gain as well as feed conversion ratio, respectively, than the control and other groups. Additionally, levels of T3, T4, total proteins, albumin, and glutathione (GSH) were significantly reduced in both G3 and G4 compared to control. However, urea, creatinine, ALT, AST, total cholesterol, triglycerides, protein carbonyl content (PCC), and malondialdehyde (MDA) were significantly increased ( P  ≤ 0.05) in cadmium and lead-exposed groups. Dietary N. oculata (4%) improves serum proteins, creatinine, urea, T4, and oxidative stress indicators as compared to the control group. Finally, 4% dietary N. oculata greatly enhances the investigated parameters in terms of performance, thyroid hormones, serum biochemical, and antioxidant activity and may assist in reducing the endocrine disrupting effects of Pb and Cd .

Oxidative stress is an imbalance between free radicals and antioxidants which leads to reactive oxygen species (ROS) production in cells. Reactive oxygen species contains oxygen radicals that easily react with other molecules in the biological system. For decades, lead acetate (Pb(C 2 H 3 O2) 2 ) is used as an additive for many widely used chemical products such as insecticides, hair dyes, and cosmetics; however, contact with lead acetate may irritate skin, eyes, and mucous membranes. In the present study, the antioxidant and anti-inflammatory effect of using ferulic acid to inhibit lead acetate-induced toxicity in rats is investigated. Lead acetate was orally given at a dose of 20 mg/kg body weight for 10 days, either alone or with ferulic acid at dose 25 mg/kg. Serum luteinizing hormone (LH), total testosterone, and follicle-stimulating hormone (FSH) levels were measured. Also, reactive oxygen species (ROS), lipid peroxidation (LPO), total antioxidant capacity (TAC), and catalase (CAT) activities were determined. In addition, histopathological changes of testes and kidney were examined. Results showed that administration of lead acetate induced oxidative stress through attenuation of luteinizing hormone, total testosterone, and follicle-stimulating hormone levels in serum. Moreover, the kidney and testes of lead acetate-treated animals exhibited elevation of ROS level, lipid peroxide levels, as well as lysosomal enzyme activity such acid phosphatase and N-acetyl-β-glucosminidase. DNA fragmentation and histological changes were also observed in lead acetate-treated group. In contrast, ferulic acid treatment reduced the deleterious effects induced by lead acetate in both testes and kidney tissues. These results illustrated that ferulic acid has a protective action against toxicity caused by lead acetate in rats. In conclusions, ferulic acid may have future therapeutic relevance in the prevention of lead acetate-induced testicular and renal toxicity in rats.

Kidneys are primarily sensitive to lead (Pb) poisoning due to their cardinal role in lead excretion. Then, we studied the effect of glutamine (Gln) on lead nephrotoxicity in rats by assessing the histopathological and biochemical parameters (the renal NF-kβ expression, metabolic profile, oxidative stress, inflammatory markers, methylglyoxal (MGO), and glyoxalase-I activity). Forty rats were allotted into four groups (ten rats in each): normal (N), Gln-treated N, Pb intoxication (Pbi), and Gln-treated Pbi. The treated groups took 0.1% Gln in drinking water for 1 month. To motivate lead poisoning, rats gained 50 mg/l lead acetate in drinking water for 1 month. Oxidative stress indices (total glutathione, its reduced and oxidized forms, their ratios, advanced protein oxidation products, malondialdehyde, and ferric ion reducing power) and inflammatory markers (renal nuclear factor-kβ expression, interleukin 1β level, and myeloperoxidase activity) were measured. Furthermore, metabolic profile (fasting blood sugar, insulin, insulin resistance, lipid profile, and atherogenic index) and renal dysfunction parameters were determined. Pb-induced renal histopathological alterations were investigated by a pathologist. In the kidney of Pbi rats, the glomerulus was damaged. Gln prevented kidney damage and reduced kidney dysfunction parameters. In addition, Gln decreased oxidative stress and inflammation in sera and kidney homogenates. In addition, it improved insulin resistance, dyslipidemia, and carbonyl stress (p < 0.001). Gln guarded the kidneys versus lead intoxication by improving insulin resistance and dyslipidemia, elevating antioxidant markers, and diminishing inflammation and carbonyl stress.

Lead, a highly toxic pollutant, causes numerous health problems and affects nearly all biological systems thus arousing interest in using antioxidants to reduce its toxic effects. Therefore, the undertaken study estimated the influence of cerium oxide nanoparticles (CeO2-NPs) on the lead acetate–induced genotoxicity and inflammation in the kidney and heart tissues of mice. Twenty male mice were randomly divided into negative control and lead acetate and/or CeO2-NPs administrated groups. Comet and diphenylamine assays were conducted to assess the DNA damage and the expression of apoptosis-related genes and inflammatory cytokines were also measured in addition to the estimation of reactive oxygen species (ROS) level. Co-administration of CeO2-NPs significantly reduced the DNA damage and ROS generation caused by lead acetate in the kidney and heart tissues. The co-administration of CeO2-NPs also ameliorated the lead acetate–induced dysregulation in the expression levels of p53, K-ras, interleukin-6, and cyclooxygenase-2 in the kidney and heart. Conclusion: the co-administration of CeO2-NPs suppresses the genotoxicity, inflammation, and ROS generation resulting from lead acetate administration and restoring the genomic DNA integrity; thus, administration of CeO2-NPs is recommended to minimize the lead acetate–induced hazards.