This study was designed to evaluate the ameliorative role of betaine on hepatic and renal dysfunction caused by acrylamide in female rats. Thirty two (32) adult female rats were randomly and equally divided into four groups (G1, G2, G3 and G4) and were treated for (65) days as following: Group G1 (Control group), G2: rats were intubated 250mg/kg B.W of betaine; animals in group G3 were intubated 1mg/kg B.W of acrylamide, in addition to acrylamide. 250mg/kg B.W of betaine were administered orally to rats in groups G4. Fasting (8-12 hrs.) blood samples were collected by cardio puncture technique at the end of the experiment, serum were collected for measuring the following parameters A: liver enzyme makers; serum activity of alanine aminotransferase (ALT), aspartate aminotransferase (AST) and alkaline phosphatase (ALP)  B; renal function parameters including: serum creatinine, urea and uric acid concentration. The hepato and renal protective effect of betaine was clarified in groups (G2 and G4) manifested by significant decrease in serum, ALT, AST and ALP activity, as well as  significant decrease in serum creatinine, urea and uric acid concentration comparing to acrylamide (G3) treated group. Such functional changes were accompanied with structural (histopathological) alteration in hepatic and renal tissue. In conclusion, the results of the current study documented the negative effect of acrylamide on liver and kidney function and documented hepatorenal protective effect of betaine.

From a health standpoint, fluoride (F) is a vital element for humans. It had harmful effects on numerous organs when consumed in high dosages. Fluoride poisoning has been linked to liver damage. The purpose of this study was to see how sodium fluoride (Naf) affected liver function and the glycemic index in adult male albino rats. Fourteen (14) adult male Wistar albino rats were randomly and evenly divided into two groups and given the following treatments for thirty (30) days: G1 Group (Control group), were given distilled water and fed a balanced diet, G2 rats were administered water that contained 100 ppm Naf. The animals were fasted for 8-12 hours before being anesthetized and blood samples were taken by heart puncture technique at zero day (zero time) and (30) day. The following parameters were measured using the serum. The glycemic index contains (glucose, insulin, and insulin resistance), as well as liver function tests such as serum activity of alanine aminotransferase (ALT), aspartate aminotransferase (AST) and gamma glutamyl transferase (GGT), as well as direct, indirect and total bilirubin concentration. The livers and pancreas were quickly delivered, meticulously dissected out, prepped, and viewed under a light microscope. The results demonstrated that 30 days of exposure to Naf in drinking water produced liver damage manifested by significant increases in blood ALT, AST, and GGT activity as well as significant elevation in serum bilirubin (direct, indirect and total) concentration compared to control group. A significant rise in blood glucose levels and a fall in blood insulin levels and IR were detected at the end of the experiments in Naf treated group when compared to the control. Histopathological changes in Naf treated group was observed in hepatic and pancreatic tissue manifested by generalised degeneration and necrosis of hepatocytes, in addition, to severe degeneration of acinar and pancreatic islet cells. In conclusion, the findings of this investigation revealed Naf therapy-induced liver damage and a change in the glycemic index in adult male rats.

The purpose of this research was to investigate the beneficial effects of phosphatidylcholine in reducing changes in both lipid and protein profiles in addition to atherogenic index in adult rats with fructose-induced metabolic syndrome. Thirty-six mature Wistar Albino female rats (Rattus norvegicus) (aged 12-15 weeks and weighing 200±10 g) were divided randomly into four groups (G1, G2, G3, and G4); then variable treatments were orally administered for 62 days as follows: G1 (Control group), received distilled water; G2, treated with phosphatidylcholine (PC) orally (1 g/kg BW); G3 (Fr), orally dosed with 40% fructose and 25% fructose mixed with drinking water; G4 (Fr+PC), were also intubated with 40% fructose and 25% fructose in drinking water, and received PC at 1 g/kg BW by oral tube. At the end of the research, specimens were taken by cardio puncture approach after fasting for 8-12 h. Serum was obtained to measure lipid criteria (total serum cholesterol, triacylglycerol, high-density lipoprotein-cholesterol, low-density lipoprotein-cholesterol, very low-density lipoprotein-cholesterol, non-high-density lipoprotein-cholesterol, and Atherogenic index) and protein profile (total protein, albumin, and globulins). The results showed that the occurrence of dyslipidaemia (hypercholesterolemia, triacyleglycerolemia) increase in low density of lipoprotein-cholesterol, very low-density lipoprotein-cholesterol, no-high density lipoprotein-cholesterol concentrations and atherogenic index and reduce the concentration of high-density lipoprotein-cholesterol) in fructose treated animals in addition to disturbance in protein profile (lowered in total protein and globulins level).PC treatment resulted in decreased changes in lipid profile, protein profile, and atherogenic index in rats, whereas fructose induced metabolic syndrome. In conclusion, using Phosphatidylcholine treatment in rats may reduce the changes of lipid and protein profiles and atherogenic index while fructose may lead to metabolic syndrome.

This study was aimed to explore the role of gallic acid (GA) in ameliorating in reducing adverse effects of cadmium chloride (CdCl2) on antioxidant status and lipid profile in adult male rats. Twenty-eight (28) adult male rats were divided randomly into four equal groups; they were daily handled for 30 days, as follows: control group (C), received tap water only. (G1), received 100ppm of CdCl2 in drinking tap water, animals in proceeding groups were given in addition to CdCl2 in drinking water the following: intraperitoneal injection of GA 100 mg/kg. daily (G2 group) and the combination of GA and CdCl2 were given to rats in group (G3) in the same pattern.  At the end of the experiment, fasting blood samples were collected and serum was isolated for measuring of antioxidant status and lipid profile. The results showed that administration CdCl2 (G1 group) caused a case of dyslipidemia illustrated by significant elevation in serum cholesterol concentration in lipoprotein low density lipoprotein-cholesterol (LDL-C) and very low-density lipoprotein-cholesterol (VLDL-C), total cholesterol (TC), triglyceride (TAG) and non-HDL-C accompanied with significant decrease in cholesterol of high density lipoprotein (HDL-C) concentrations. The results also revealed a significant elevation in lipid indices including, coronary risk index (CRI), and cardiovascular risk index (CVRI) in CdCl2 exposed rats. While significant elevation in malondialdehyde (MDA) and reduction in (GSH) concentrations observed in the same group comparing to gallic acid and control group, indicating a case of oxidative stress. The current results also recorded that intraperitoneal injection of GA against CdCl2 caused amelioration of all previously estimated parameters.