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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 acetate (PbAc) is one of the top five most dangerous toxic heavy metals, particularly leading to kidney damage and posing serious health risks in both humans and animals. Sinapic acid (SNP) is a naturally occurring flavonoid found in fruits and vegetables that stands out with its antioxidant, anti-inflammatory, and anticancer properties. This is the first study to investigate the effects of SNP on oxidative stress, inflammation, apoptosis, autophagy and endoplasmic reticulum (ER) stress in PbAc-induced nephrotoxicity in rats by biochemical, molecular and histological methods. 35 Spraque dawley rats were randomly divided into five groups of 7 rats each: control, PbAc, SNP (10mg/kg), PbAc + SNP 5, PbAC + SNP 10. PbAc at a dose of 30 mg/kg body weight was administered via oral gavage alone or in combination with SNP (5 and 10 mg/kg body weight) via oral gavage for seven days. While PbAc impaired renal function by increasing serum urea and creatinine levels, SNP decreased these levels and contributed to the improvement in renal function. The administration of SNP reduced oxidative stress by increasing PbAc-induced decreased antioxidant enzyme (SOD, CAT, and GPx) activities and GSH levels, decreasing MDA levels, a marker of increased lipid peroxidation. SNP administration reduced NF-κB, TNF-α, IL-1β, NLRP3, and RAGE mRNA transcription levels, NF-κB, and TNF-α protein levels that are among the PbAc-induced increased inflammation parameters. Decreases in antiapoptotic Bcl-2 and increases in apoptotic Bax, APAF-1, and Caspase-3 due to PbAc exposure, SNP reversed the situation. SNP reduced ER stress caused by PbAc by increasing PERK, IRE1, ATF-6, CHOP, and GRP-78 levels and made it tend to regress. SNP reduced autophagy damage by decreasing the Beclin-1 protein level increased by PbAc. The findings of the present study suggested that SNP attenuates PbAc-induced nephrotoxicity. Graphical abstract

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.

Neuroimmune alterations have important implication in the neuropsychiatric symptoms and biochemical changes associated with lead-induced neurotoxicity. It has been suggested that inhibition of neuroinflammatory-mediated lead-induced neurotoxicity by phytochemicals enriched with antioxidant activities would attenuate the deleterious effects caused by lead. Hence, this study investigated the neuroinflammatory mechanism behind the effect of Ginkgo biloba supplement (GB-S) in lead-induced neurotoxicity in mice brains. Mice were intraperitoneally pretreated with lead acetate (100 mg/kg) for 30 min prior the administration of GB-S (10 and 20 mg/kg, i.p.) and ethylenediaminetetraacetic acid (EDTA) (50 mg/kg, i.p.) for 14 consecutive days. Symptoms of neurobehavioral impairment were evaluated using open field test (OFT), elevated plus maze (EPM), and tail suspension test (TST) respectively. Thereafter, mice brain hippocampi were sectioned for myeloperoxidase activity (MPO), pro-inflammatory cytokine (TNF-α and IL-6) estimation and inflammatory protein (NF-κB) expression. Furthermore, histomorphormetric studies (Golgi impregnation and Cresyl violet stainings) were carried out. GB-S (10 and 20 mg/kg) significantly restores neurobehavioral impairments based on improved locomotion, reduced anxiety- and depressive-like behavior. Moreover, GB-S reduced the MPO activity, inhibits TNF-α, IL-6 release, and downregulates NF-κB immunopositive cell expression in mice hippocampus. Histomorphometrically, GB-S also prevents the loss of pyramidal neuron in the hippocampus. The endpoint of this findings suggest that GB-S decreases neuropsychiatric symptoms induced by lead acetate through mechanisms related to inhibition of release of pro-inflammatory mediators and suppression of hippocampal pyramidal neuron degeneration in mice.

Lead (Pb) is an environmental toxicant; its consumption can induce renal deficits. In this study, we explored the possible protective efficiency of Moringa oleifera extract (MOE) against lead acetate (PbAc)-mediated reprotoxicity. Four experimental groups of seven rats each were used: control, PbAc, MOE, and MOE+PbAc groups. All groups were given their respective treatment for 4 weeks. PbAc impaired the oxidative/antioxidative balance in the renal tissue, as shown by the decreased antioxidant proteins (glutathione, glutathione reductase, glutathione peroxidase, catalase, and superoxide dismutase) and increased oxidants (lipid peroxidation and nitric oxide). Additionally, PbAc enhanced the progression of kidney inflammation by increasing tumor necrosis factor-alpha, interleukin-1 beta, and nuclear factor kappa B associated with upregulation of inducible nitric oxide synthase. Moreover, a dysregulation in the apoptotic-regulating proteins (Bax, caspase-3, and Bcl2) were recorded upon PbAc exposure. Remarkably, MOE oral administration restored redox homeostasis, suppressed the inflammatory and apoptotic responses in the kidney tissue. Our findings point out that MOE could be used as an alternative remedy to overcome the adverse effects of Pb exposure, which may be due to its potent antioxidant, anti-inflammatory, and anti-apoptotic effects.

Lead, toxic heavy metal of global concern, induces toxicity in various organs via oxidative stress. Thereby, in this study, the protective role of curcumin against lead acetate-induced toxicity was evaluated. Thirty-two male albino rats were allocated equally into four groups and orally administered with corn oil as a vehicle (Cont.), curcumin (CUR) (400 mg/kg bw), lead acetate (LA) (100 mg/kg bw), and lead acetate plus curcumin (LA + CUR). All rats had received their treatments daily for 4 weeks. The results revealed that LA toxicity induced normocytic normochromic anemia with significant leukocytosis and lymphocytosis. Moreover, LA-intoxicated rats showed a marked elevation in the liver enzyme activities, serum cholesterol, and triglyceride levels. In contrast, sero-immunological parameters, total protein, albumin, globulin, and testosterone levels were significantly reduced compared to the control rats. Additionally, LA-induced hepatic and testicular oxidative damage revealed by marked increased in MDA level with prominent reduction in the antioxidant system. The gene expression of the hepatic pro-inflammatory markers and testicular steroidogenic biomarkers including LHR and aromatase were significantly upregulated; meanwhile, the expressions of testicular StAR, CYP17a, 3B-HDS, SR-B1, and P450SCC were significantly downregulated in the LA-intoxicated group. Curcumin treatment could partially improve the hematological, biochemical, and histopathological alterations induced by LA. Also, it was observed that curcumin significantly restored hepatic pro-inflammatory markers and testicular steroidogenic enzymes. In conclusion, curcumin has antioxidant, anti-inflammatory, and immunomodulatory effects and is able to minimize the LA-induced oxidative damage in rats.

Lead acetate (PbAc) is one of the toxic metals in the environment which causes many effects on different organs of the body. And due to the importance of the olive tree, with its healthy and protective elements against many diseases, the leaf extract of this tree was chosen in our study. Therefore, the aim of this study was to investigate the role of olive leaf ( Olea europea L.) extract (OLE) against PbAc-induced sperm toxicity, sex hormone changes, oxidative stress, and histopathological changes in rats. Twenty male Wistar rats were divided into four groups (group 1, as control; group 2, OLE; group 3, PbAc; group 4, PbAc+OLE). In the PbAc group, the body weight, testis and epididymis weights, sexual hormones, sperm characteristics, GR, GPx, GST, GSH, SOD, and CAT were significantly decreased, and the sperm abnormality and TBARS level were significant increase when compared with control and OLE groups. Also, numerous damages to testicular tissue were observed in the PbAc group when compared to the control group, while the treatment with OLE in the fourth group led to improvement of sex hormones, semen characteristics, oxidative stress, and testicular tissue damage caused by PbAc. It can be concluded that OLE has a protective and ameliorative effects against PbAc-induced oxidative stress, apoptosis and alterations in testicular tissue, and sperm quality in rats.

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.

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 (100 g/kg), LA + MYC (100 mg/kg), LA + MYC (200 mg/kg), LA + FST (100 mg/kg) and LA + FST (200 mg/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.

Lead is one of the utmost contaminated and dangerous heavy metals. This toxicant ultimately enters into the human body through the food chain and accumulated in the body because the animal/human body has not an appropriate mechanism to excrete it from the body. The main objective of the present research was to assess the toxicological effects of lead on body weights, biochemical, and hematological parameters of chickens and also to measure its bioaccumulation in the brain. Lead acetate was administrated orally at doses of 0, 71, 142, 213, and 284 mg/kg of body weight of chicken for groups A, B, C, D, and E, respectively. Along with determination of biometry of all experimental chicks, hematological [hemoglobin (Hb), packed cell volume (PCV), mean corpuscular hemoglobin concentration (MCHC), total erythrocyte count (TEC), white blood cells (WBCs), leukocyte differential count (LDC)] and biochemical [low density lipoprotein (LDL), total protein, high-density lipoprotein (HDL), and alanine aminotransferase (ALT)] parameters were measured. The present study showed that the bodyweight of chickens was not affected significantly by lead acetate exposure. The levels of MCHC, PCV, TEC, Hb, LDL, HDL, and total protein were found to be significantly decreased while WBC, LDC, and ALT profile were enhanced due to administration of lead acetate. Bioaccumulation of lead acetate was found to be higher in the brain. We conclude that the chronic administration of lead acetate affected the blood and biochemical profile of exposed chicken. These effects might be due to the accumulation of the chemical in certain vital organ(s). However, further studies in the future are suggested to refine such findings.