Lead (Pb(2+)) toxicity is the most common form of heavy metal intoxication in humans and animals. Therefore, the current study was conducted to evaluate the potential ameliorative effects of curcumin on lead acetate (LA)-induced deleterious effects in the liver and kidney. Forty male Wistar rats were divided into four equal groups; first group was used as a control and given both corn oil orally and vehicle of lead acetate intraperitoneally (i.p). Groups from 2-4 were treated with lead acetate (LA; 50 mg/kg BW i.p), curcumin (200 mg/kg BW orally), and curcumin plus lead acetate, respectively. Curcumin was administered 3 weeks before LA injection for 7 days. Pb(2+)-intoxicated rats have higher Pb(2+) levels compared to other treated groups. Results revealed that lead acetate significantly increased the serum levels of hepatic transaminases (GPT and GOT), urea and creatinine, while albumin was significantly decreased. In parallel, serum IgG, IgM, and IgA were significantly decreased in LA-injected rats. LA groups showed decrease in messenger RNA (mRNA) expression of catalase, SOD, GST, GPx, and alpha-1 acid glycoprotein (AGP), while the gene expression of desmin, vimentin, transforming growth factor-β1 (TGF-β1), monocyte chemoattractant protein-1 (MCP-1), and alpha-2 macroglobulin (α-2M) was increased. Prior and coadministration of curcumin with LA for 7 days significantly improved the ameliorated changes in liver and kidney, immunoglobulins, and mRNA expression. Moreover, curcumin ameliorated LA-induced congestion of hepatic and renal blood vessels and decreased fibrous tissue proliferation and necrosis of hepatocytes. In the kidney, LA-induced degeneration in tubular epithelium and intraluminal hyaline casts and prior curcumin administration restored normal renal structure with mild congestion of renal blood vessels. The results clarify the potential of curcumin to counteract the immunosuppressive alteration in gene expression as well as hepatic and renal damage occurred after Pb(2+) intoxication.

Cadmium (Cd) is the most prevalent toxic metal present in livestock feed; therefore, the present study aimed to examine the ameliorative effects of grape seed extract (GSE) on cadmium chloride (CdCl2)-induced testicular dysfunction of Wistar rats. Male adult Wistar rats (40 rats; n=10/group) were divided into four equal groups. Group one was used as a control, and was given ad libitum access to food and water. Groups 2–4 were treated with CdCl2 [5 mg/kg body weight (BW)], GSE (400 mg/kg BW, orally), and GSE plus CdCl2, respectively. Blood and testicular tissues were collected and assayed for biochemical and histopathological changes, respectively. Testicular genes were expressed using semi-quantitative RT-PCR analysis. The results of the present study demonstrated that there was a decrease in serum testosterone levels following CdCl2 toxicity, which were normalized after GSE co-administration. Furthermore, CdCl2 significantly increased the serum levels of malondialdehyde, and decreased levels of antioxidants. At the histopathological level, the testes of the CdCl2 group exhibited congestion, edema in the interstitial blood vessels, irregular arrangement of the epithelial lining of the seminiferous tubules, and degeneration and sloughing of the spermatogenic cells, which accumulated in the center of the seminiferous tubules. Such pathological alterations were ameliorated following treatment with GSE in the CdCl2 plus GSE group. The immunohistochemical expression of B-cell lymphoma 2-associated X protein was high in the CdCl2 group, and low in the control and GSE groups. Co-treatment with GSE and CdCl2 exhibited ameliorative effects on the immunoreactivity of B-cell lymphoma 2-associated X protein. CdCl2 toxicity induced a significant downregulation in the mRNA expression levels of cytochrome P450 cholesterol side-chain cleavage enzyme, cytochrome P450 17A1, 3β-hydroxysteroid dehydrogenase (3β-HSD), 17β-HSD, androgen receptor, steroidogenic acute regulatory protein, and follicle-stimulating hormone receptor. GSE administration exhibited a stimulatory effect on steroidogenesis-associated enzymes, and co-treatment with GSE and CdCl2 normalized and upregulated the mRNA expression levels of these examined genes. This study concluded that GSE has beneficial protective effects against the deleterious effects of CdCl2 on the testis.

ABSTRACT. Leptin is a protein synthesized and secreted primarily by adipocytes, and the circulating leptin concentration is elevated in obese humans and rodents. Recently, we have established a sandwich enzyme-linked immunosorbent assay for canine leptin. In the present study, plasma leptin concentrations were measured in experimentally developed obese beagles and in clinically obese dogs. When 5 male beagles were given a high-energy diet for 3 months, all of them became obese and the plasma leptin concentration significantly increased from 2.4 ± 1.2 to 4.9 ± 0.9 ng/ml, positively correlating with body fat content estimated by the deuterium oxide dilution method (r=0.87). The leptin concentrations of plasma samples collected from 59 dogs in veterinary practices were compared with their body condition scores (BCS). The plasma leptin concentrations of obese dogs were 9.7 ± 0.7 and 12.3 ± 1.5 ng/ml at BCS=4 and BCS=5, respectively, which were significantly higher than those of optimal (BCS=3) dogs (2.7 ± 0.3 ng/ml). There was no significant effect of sex and breed. A weak positive correlation (r=0.37) was found between the plasma leptin concentration and age, probably due to the lesser content of visceral fat in puppies younger than 1 year old. These results indicate that plasma leptin is a good index of adiposity in dogs regardless of breed, age and sex, and may be useful for quantitative assessment of obesity in small animal practice.

No abstract

Leptin is an adipose tissue-derived cytokine plays key roles in the regulation of food intake and energy expenditure. However, regulatory mechanisms of leptin gene expression are not fully elucidated in ruminants that utilize short-chain fatty acids (SCFA), known as volatile fatty acids, as principal energy sources. In this study, we determined effects of SCFA and long-chain fatty acids (LCFA) on leptin expression in bovine adipocytes. Bovine stromal vascular cells isolated from subcutaneous adipose tissue of Holstein cows were cultured to confluence and treated sequentially with dexamethasone and isobutylmethylxanthine for 2 days and insulin and troglitazone for 12 days to achieve full differentiation to adipocytes. The cells started to accumulate lipids 4 days after the onset of treatment, with increased mRNAs expression of leptin, as well as aP2, adiponectin, and PPAR-γ  Removal of fetal calf serum and reduction of glucose in the culture medium of differentiated adipocytes decreased leptin mRNA expression.Subsequent addition of acetate, butyrate, or propionate dose-dependently restored and rather increased leptin expression, while addition of LCFA suppressed it. The stimulatory effect of acetate was abolished by prior treatment of the cells with pertussis toxin and by addition of LCFA. Furthermore, cows fasted for 48h and fed thereafter, elaborate reduced and increased plasma leptin levels, respectively. Thus, these results suggest that plasma leptin levels in cows are inversely controlled at transcription by VFA and LCFA, and that the effects of SCFA possibly act through a G protein-coupled receptor for SCFA.

A new preservation approach is presented in this article to prolong the lifetime of raw chicken meat and enhance its quality at 4 °C via coating with highly soluble kidney bean protein hydrolysate. The hydrolysates of the black, red, and white kidney protein (BKH, RKH, and WKH) were obtained after 30 min enzymatic hydrolysis with Alcalase (E/S ratio of 1:100, hydrolysis degree 25–29%). The different phaseolin subunits (8S) appeared in SDS-PAGE in 35–45 kD molecular weight range while vicilin appeared in the molecular weight range of 55–75 kD. The kidney bean protein hydrolysates have considerable antioxidant activity as evidenced by the DPPH-scavenging activity and β-carotine-linolenic assay, as well as antimicrobial activity evaluated by disc diffusion assay. BKH followed by RKH (800 µg/mL) significantly (p ≤ 0.05) scavenged 95, 91% of DPPH and inhibited 82–88% of linoleic oxidation. The three studied hydrolysates significantly inhibited the growth of bacteria, yeast, and fungi, where BKH was the most performing. Kidney bean protein hydrolysates could shield the chicken meat because of their amphoteric nature and many functional properties (water and oil-absorbing capacity and foaming stability). The quality of chicken meat was assessed by tracing the fluctuations in the chemical parameters (pH, met-myoglobin, lipid oxidation, and TVBN), bacterial load (total bacterial count, and psychrophilic count), color parameters and sensorial traits during cold preservation (4 °C). The hydrolysates (800 µg/g) significantly p ≤ 0.05 reduced the increment in meat pH and TVBN values, inhibited 59–70% of lipid oxidation as compared to control during 30 days of cold storage via eliminating 50% of bacterial load and maintained secured storage for 30 days. RKH and WKH significantly (p ≤ 0.05) enhanced L*, a* values, thus augmented the meat whiteness and redness, while, BKH increased b* values, declining all color parameters during meat storage. RKH and WKH (800 µg/g) (p ≤ 0.05) maintained 50–71% and 69–75% of meat color and odor, respectively, increased the meat juiciness after 30 days of cold storage. BKH, RKH and WKH can be safely incorporated into novel foods.

BackgroundAn overdose of paracetamol is a frequent reason for liver and renal toxicity and possible death and curcumin has hepatoprotective properties against liver damage. The exact mechanism of such protection is not clear. Therefore, this study was conducted to examine the molecular levels of the protective effect of curcumin on paracetamol overdose induced hepatic toxicity in rats.MethodsMale Wistar rats were allocated into 4 groups. Control group, administered corn oil; curcumin group, administered curcumin (400 mg/kg BW daily intra-gastric) dissolved in corn oil; paracetamol group, administered corn oil with a single dose of paracetamol (500 mg/kg BW intra-gastric) and protective group, administered curcumin with a single dose of paracetamol. Curcumin was administered for 7 successive days, while paracetamol was administered at day six of treatment. Blood and liver tissues were collected for biochemical, histopathological, immunohistochemical and molecular examination.ResultsSerum analysis revealed an alteration in parameters of kidney and liver. A decrease in the antioxidant activity of liver was recorded in paracetamol group while curcumin administration restored it. Histopathological findings showed an extensive coagulative necrosis in hepatocytes together with massive neutrophilic and lymphocytic infiltration. Immunostaining of liver matrix metalloproteinase-8 (MMP-8) in paracetamol administered rats showed an increase in MMP-8 expression in the area of coagulative necrosis surrounding the central vein of hepatic lobules. Curcumin administration decreased MMP-8 expression in liver of paracetamol administered rats. Gene expression measurements revealed that paracetamol decreased the expression of antioxidant genes and increased the expression of interleukin-1β (IL-1β), IL-8, tumor necrosis factor-α (TNF-α) and acute phase proteins. Curcumin administration ameliorated paracetamol-induced alterations in genes expression of antioxidant and inflammatory cytokines.ConclusionThe results clarified the strong protective effect of curcumin on paracetamol induced hepatic toxicity in rats at the immunohistochemical and molecular levels.

Highlights Biological ZnONPs have considerable bactericidal against pathogenic fish bacteria. Biological ZnONPs reduced the bacterial load in water and fish tissues. Biological ZnONPs enhanced FCR feeding and swimming behaviors. Biological ZnONPs stimulated fish health and production.