Sediment toxicity and heavy metals in the Kattegat and Skaggerak

Superficial (0 to 2 cm) sediments were sampled from 62 sites in Kattegat and Skagerrak during autumn 1989 and spring 1990, tested for toxicity to Daphnia magna and Nitocra spinipes (Crustacea) and analyzed for heavy metals (Cd, Cr, Cu, Hg, N, Pb, Zn), nutrients (N and P) and organic carbon. Whole sediment toxicity to Nitocra spinipes, expressed as 96-h LC50, ranged from 1.8 to > > 32 percent sediment (wet wt), which is equivalent to 0.63 to 53 percent dry wt. Sediment total metal concentrations (mg kg^-1 dry wt) ranged from 0.01 to 0.32 for Cd, 8 to 57 for Cr, 3 to 40 for Cu, 0.03 to 0.86 for Hg, 3 to 43 for Ni, 6 to 37 for Pb and 21 to 156 for Zn. Analyzed concentrations of heavy metals were tested for correlation with whole sediment toxicity normalized to dry wt, and significant correlations (Spearman p<0.05) were found for Cd, Cr, Cu, Hg, and Ni. However, the analyzed concentrations of these metals were below the spiked sediment toxicity of these heavy metals to N. spinipes, except for Cr and Zn for which analyzed maximum concentrations approached the 96-h spiked sediment LC50s. There was no improvement in correlation between the sum of heavy metal concentrations normalized to their spiked toxic concentrations (Toxic Unit approach) and the whole sediment toxicity. Calculated heavy-metal-derived toxicity based on toxic units and whole sediment toxicity ranged from 0.1 to 24 (mean value 2.3 and SD 4.2). Theoretically, a value of 1.0 would explain whole sediment toxicity from measured metal concentrations using this approach. Thus, in spite of the fact that the total concentrations of the heavy metals were sufficient to cause toxicity based on an additive model for most of these sediments, the observed toxicity of the sediments from Kattegat and Skagerrak could not exclusively be explained by the concentrations of heavy metals, except for Cr and Zn at their maximum concentrations. Therefore, other pollutants than these heavy metals must also be considered as possible sediment toxicants.     

Morin Attenuates Neurochemical Changes and Increased Oxidative/Nitrergic Stress in Brains of Mice Exposed to Ketamine: Prevention and Reversal of Schizophrenia-Like Symptoms

Previous studies have revealed that morin (MOR), a neuroactive bioflavonoid, with proven psychotropic and neuroprotective properties reduced schizophrenic-like behaviors in mice. This study further evaluated the ability of MOR to prevent and reverse ketamine-induced schizophrenic-like behaviors and the underlying neurochemical changes and increased oxidative/nitrergic stress in mice. In the preventive protocol, mice received intraperitoneal injection of MOR (100 mg/kg), reference antipsychotic drugs [haloperidol (1 mg/kg), risperidone (0.5 mg/kg)], or saline daily for 14 consecutive days prior to i.p. injection of ketamine (KET) (20 mg/kg/day) from the 8th to the 14th day. In the reversal protocol, the animals received KET or saline for 14 days prior to MOR, haloperidol, risperidone, or saline treatments. Schizophrenic-like behaviors: positive (open-field test), negative (social-interaction test) and cognitive (Y-maze test) symptoms were evaluated. Thereafter, the brain levels of dopamine, glutamate, 5-hydroxytryptamine and acetyl-cholinesterase, as well as biomarkers of oxidative/nitrergic stress were measured in the striatum, prefrontal-cortex (PFC) and hippocampus (HC). Morin prevented and reversed KET-induced hyperlocomotion, social and cognitive deficits. Also, MOR or risperidone attenuated altered dopaminergic, glutamatergic, 5-hydroxytryptaminergic and cholinergic neurotransmissions in brain region-dependent manner. The increased malondialdehyde and nitrite levels accompanied by decreased glutathione concentrations in the striatum, PFC and HC in KET-treated mice were significantly attenuated by MOR or risperidone. Taken together, these findings suggest that the anti-schizophrenic-like activity of MOR may be mediated via mechanisms related to attenuation of neurochemical changes and oxidative/nitrergic alterations in mice.     

Aggressive-like behaviour and neurocognitive impairment in alcohol herbal mixture-fed mice are associated with increased neuroinflammation and neuronal apoptosis in the prefrontal cortex

Alcohol-induced aggression and related violence is a serious and common social problem globally. Alcohol use is increasingly found in the form of alcoholic herbal mixtures (AHM) with indiscriminate and unregulated alcohol content. This study investigated the effects of AHM on aggressive-like, neurocognitive impairment and brain biochemical alteration in mice. Thirty-two male resident mice were paired housed with female mice for 21 days in four groups (n = 8). Resident mice were treated orally with normal saline, AHM, ethanol and AHM + ethanol daily for 14 days. Aggressive-like behaviour was scored based on the latency and frequency of attacks by the resident mouse on the intruder. Neurocognitive impairment was determined using the Y-maze test (YMT) and novel object recognition test (NORT). Acetylcholinesterase, glutamic acid decarboxylase (GAD), pro-inflammatory and oxidative stress parameters were determined in the prefrontal cortex (PFC). Neuronal morphology, cytochrome c (Cyt-c) and nuclear factor-kappa B (NF-ĸB) expressions were determined. AHM and in combination with ethanol showed an increased index of aggression typified by frequency of attack and reduced latency to attack when compared to normal saline-treated animals. Co-administration of AHM and ethanol significantly reduced cognitive correct alternation (%) and discrimination index in the YMT and NORT, respectively. AHM and ethanol increased acetylcholinesterase, Pro-inflammatory cytokines and oxidative stress parameters while they reduced GAD. There were significantly reduced neuronal counts and increased expression of Cyt-c and NF-ĸB, respectively Alcoholic herbal mixture increased aggressiveness and caused neurocognitive impairment via increased oxido-inflammatory stress in the prefrontal cortex.     

The Anti-Parkinson Potential of Gingko biloba-Supplement Mitigates Cortico-Cerebellar Degeneration and Neuropathobiological Alterations via Inflammatory and Apoptotic Mediators in Mice

Neurochemical Research - Activation of nuclear factor erythroid 2 related factor 2 (Nrf2) associated with the suppression of various oxido-inflammatory pathways and the controller of several gene...     

d-Ribose–l-cysteine exhibits adaptogenic-like activity through inhibition of oxido-inflammatory responses and increased neuronal caspase-3 activity in mice exposed to unpredictable chronic mild stress

Molecular Biology Reports - Adaptogens are substances that act nonspecifically to combat stress by regulating the key elements involved in stress-induced pathologies. d-Ribose–l-cysteine...     

Molecular mechanisms involved in the prevention and reversal of ketamine-induced schizophrenia-like behavior by rutin: the role of glutamic acid decarboxylase isoform-67, cholinergic,Nox-2-oxidative stress pathways in mice

Molecular Biology Reports - Mounting evidences have shown that nicotinamide adenine dinucleotide phosphate oxidase-2 (Nox-2) pathway modifies glutamic-acid decarboxylase-67 (GAD67) (GABAergic...