Deltamethrin-induced oxidative damage and biochemical alterations in rat and its attenuation by Vitamin E
Deltamethrin is a synthetic pyrethroid insecticide used worldwide in agriculture, home pest control, protection of foodstuff and disease vector control. The objective of this study was to investigate the propensity of deltamethrin to induce oxidative stress and changes in biochemical parameters and enzyme activities in male rats following a short-term (30 days) oral exposure and its possible attenuation by Vitamin E (Vit. E). Rats were assigned to 1 of 4 treatment groups: 0 mg Vit. E and 0 mg deltamethrin/kg body weight (BW) (control); 100 mg Vit. E/kg BW; 1.28 mg deltamethrin/kg BW; 100 mg Vit. E plus 1.28 mg deltamethrin/kg BW. Results obtained showed that deltamethrin significantly (P < 0.05) induced thiobarbituric acid-reactive substances (TBARS; the marker of lipid peroxidation) in plasma. The activities of glutathione S-transferase (GST) and superoxide dismutase (SOD) were significantly decreased due to deltamethrin administration. On the other hand, treatment with Vitamin E alone increased the activities of GST and SOD, and decreased the levels of TBARS. Also, Vitamin E alleviated the harmful effect of deltamethrin in the combination group. Enzymatic activities of aminotransferases (AST and ALT), phosphatases (AcP and AlP) and lactate dehydrogenase (LDH) in plasma were significantly increased, while acetylcholinesterase (AChE) was inhibited. Deltamethrin significantly (P < 0.05) increased the levels of plasma total lipid (TL), cholesterol, triglyceride (TG), low density lipoprotein (LDL) and very low density lipoprotein (VLDL), while the level of high density lipoprotein (HDL) decreased. Vitamin E alone decreased the levels of lipids and lipoproteins, and alleviated the harmful effects of deltamethrin. Concentrations of glucose, urea, creatinine and total bilirubin were increased. While, plasma total protein (TP), albumin (A) and globulin (G) were significantly (P < 0.05) decreased. The present study revealed that the presence of Vitamin E could diminish the adverse effects of deltamethrin on most of biochemical parameters, lipid peroxidation and enzyme activities in rats. 
Functional and Biochemical Alterations of the Medial Frontal Cortex in Obsessive-Compulsive Disorder
Context The medial frontal cortex (MFC), including the dorsal anterior cingulate and the supplementary motor area, is critical for adaptive and inhibitory control of behavior. Abnormally high MFC activity has been a consistent finding in functional neuroimaging studies of obsessive-compulsive disorder (OCD). However, the precise regions and the neural alterations associated with this abnormality remain unclear.
Objective To examine the functional and biochemical properties of the MFC in patients with OCD.
Design Cross-sectional study combining volume-localized proton magnetic resonance spectroscopy and functional magnetic resonance imaging with a task encompassing inhibitory control processes (the Multi-Source Interference Task) designed to activate the MFC.
Setting Healthy control participants and OCD patients recruited from the general community.
Participants Nineteen OCD patients (10 males and 9 females) and 19 age-, sex-, education-, and intelligence-matched control participants recruited from the general community.
Main Outcome Measures Psychometric measures of symptom severity, Multi-Source Interference Task behavioral performance, blood oxygen level–dependent activation, and proton magnetic resonance spectroscopy brain metabolite concentrations.
Results Multi-Source Interference Task behavioral performance did not differ between OCD patients and control subjects. Reaction time interference and response errors were correlated with blood oxygen level–dependent activation in the dorsal anterior cingulate region in both groups. Compared with controls, OCD patients had greater relative activation of the supplementary motor area and deactivation of the rostral anterior cingulate during high- vs low-conflict (incongruent > congruent) trials. Patients with OCD also showed reduced levels of neuronal N-acetylaspartate in the dorsal anterior cingulate region, which was negatively correlated with their blood oxygen level–dependent activation of the region.
Conclusions Hyperactivation of the MFC during high- vs low-conflict conditions in patients with OCD may be a compensatory response to a neuronal abnormality in the region. This relationship may partly explain the nature of inhibitory control deficits that are frequently seen in this group and may serve as a focus of future treatment studies. 
Neurologic manifestations of diabetic comas: Correlation with biochemical alterations in the brain
Coma and other neurologic abnormalities are present in patients with either diabetic ketoacidosis (DKA) or nonketotic coma (NKC), and the cause of such phenomena are not known. Patients with NKC also manifest seizures and focal neurologic changes. Treatment of diabetic coma with insulin may induce cerebral edema by as yet undefined mechanism(s). In patients with DKA, cerebral oxygen utilization is impaired, and there is hyperviscosity of the blood. A substantial part of the brain’s energy source is derived from ketones, which in themselves can depress sensorium. Extracellular hyperosomolality is present, which may also contribute to the genesis of coma. In addition, most keto-acidotic patients have associated medical conditions, which may further impair consciousness. Biochemical changes in the brains of animals with DKA include impairment of both phosphofructokinase activity and pyruvate oxidation, and accumulation of citrate. The net effect upon sensorium in ketoacidotic patients probably represents the interaction of most of the above factors and differs markedly among individuals. Patients with NKC manifest not only depression of sensorium, but also focal motor seizures, hemiparesis, and other neurologic changes, such as aphasia, hypereflexia, sensory defects, autonomic changes, and brainstem dysfunction. Most of the aforementioned changes revert to normal after correction of hyperosomolality. Gamma amino butyric acid, which has been shown to elevate the seizure threshold, is normal in brains of ketoacidotic animals, but may be low in nonketotic coma. Also, hyperosomolality per se may produce seizures. Cerebral edema may complicate the treatment of either DKA or NKC. The available experimental evidence suggests that many of the commonly held theories for the production of such brain swelling probably do not occur. There is no breakdown of the sodium pump, sorbitol or fructose do not accumulate in brain, and brain glucose is only about 25% of that in plasma. Cerebral edema is probably produced largely by a direct action of insulin on brain at a time when plasma glucose is approaching normal values. Cerebral edema can thus theoretically be avoided by stopping insulin when plasma glucose has been lowered to values approaching normal. 
Biochemical Changes Induced by the Toxicity of Variable Sizes of Silver Nanoparticles
Background: Silver nanoparticles (SNPs) rapid involvement in industry and nanomedicine increased human exposure to variable forms of these particles, with possible potential risk on human health.
Aims: The aim of this study is to investigate the biochemical changes induced by variable sizes of SNPs toxicity.
Place and Duration of Study: Faculty of Medicine, The University of Jordan and the College of Applied Medical Sciences at Aljouf University, Saudi Arabia, between January 2013 and January 2014.
Study Design: Forty-two male mice were subjected to a daily single dose (1mg/kg body weight) of SNPs using five different sizes (10 nm, 20 nm, 40 nm, 60 nm and 100 nm) for 35 days.
Methodology: Biochemical changes of the following eleven biochemical tests were determined: aspartate aminotransferase, alanine aminotransferase, alkaline phosphatase, triglycerides, total bilirubin, creatinine, total protein, albumin, urea, uric acid and total cholesterol.
Results: Silver nanoparticles significantly elevated aspartate aminotransferase, alanine aminotransferase, alkaline phosphatase, triglycerides, total bilirubin and creatinine, with no significant change in total protein level while albumin and total cholesterol levels were lowered.
Conclusion: The findings indicate that exposure to SNPs produced significant biochemical changes that might affect the functions of the vital organs. Moreover, these alterations were size-dependent with smaller particles (10 nm and 20 nm) induced more alterations than the larger ones. 
Alterations in Biochemical Indices and Antioxidant Status in Rats Following Treatment with Gatifloxacin
Aim: Gatifloxacin (GTX) – an 8-methoxy fluoroquinolone antibacterial agent has been considered very effective in the treatment of respiratory and urinary tract infections. This study investigates the toxic potentials of GTX in Wistar rats.
Methodology: Twenty male rats (180-220 g) were randomised into four groups: I-Control, II-4 mg/kg body weight (b.w.) GTX, III-8 mg/kg b.w GTX, and IV-16 mg/kg b.w GTX.
Results: After seven days of GTX administration, the levels of plasma creatinine, urea and bilirubin were increased significantly (P<0.05) in GTX-treated rats compared to control. ALP, ALT, AST and GGT activities were also elevated significantly in the plasma of the treated animals relative to control. Similarly, hepatic malondialdehyde level increased significantly in the GTX-treated groups relative to control. Hepatic levels of ascorbic acid, reduced glutathione as well as activities of hepatic GST, catalase, and SOD were reduced significantly in a dose dependent manner in the GTX-treated animals compared to control. Besides, histopathological studies revealed very mild, moderate and severe hepatic portal congestion and cellular infiltration by mononuclear cells by the three doses of GTX.
Conclusion: Overall, three different doses of Gatifloxacin (half-therapeutic, therapeutic and double-therapeutic) induced renal and hepatic damages, as well as oxidative stress in rats. 
 Yousef, M.I., Awad, T.I. and Mohamed, E.H., 2006. Deltamethrin-induced oxidative damage and biochemical alterations in rat and its attenuation by Vitamin E. Toxicology, 227(3), pp.240-247.
 Yücel, M., Harrison, B.J., Wood, S.J., Fornito, A., Wellard, R.M., Pujol, J., Clarke, K., Phillips, M.L., Kyrios, M., Velakoulis, D. and Pantelis, C., 2007. Functional and biochemical alterations of the medial frontal cortex in obsessive-compulsive disorder. Archives of general psychiatry, 64(8), pp.946-955.
 Guisado, R. and Arieff, A.I., 1975. Neurologic manifestations of diabetic comas: correlation with biochemical alterations in the brain. Metabolism, 24(5), pp.665-679.
 Jarrar, Q., Battah, A., Obeidat, F. and Battah, K. (2014) “Biochemical Changes Induced by the Toxicity of Variable Sizes of Silver Nanoparticles”, Journal of Pharmaceutical Research International, 4(24), pp. 2670-2678. doi: 10.9734/BJPR/2014/14666.
 Olayinka, E., Ore, A. and Adeyemo, O. (2015) “Alterations in Biochemical Indices and Antioxidant Status in Rats Following Treatment with Gatifloxacin”, Journal of Pharmaceutical Research International, 6(5), pp. 293-305. doi: 10.9734/BJPR/2015/16210.