Abstract
The aim of this study was to determine the prevention of cadmium toxicity by ceftriaxone plus sulbactam with VRP1034 drug on hematological, biochemical, lipid per-oxidation, antioxidant enzymatic activities and Cd, Zn and Fe levels in the blood and tissues of cadmium exposed rats. Twenty four male rats were divided into three groups of eight rats each. Control group received distilled water where as group II received CdCl2 (1.5 mg/4 ml body weight) through gastric gavages for 21 days. Group III was received CdCl2 plus treated with ceftriaxone plus sulbactam with VRP1034 for 21 days. These parameters were measured in plasma and tissues (brain, liver and kidney) of all groups. Our findings showed that a significantly decreased cadmium (p<0.001), malonaldialdehyde (p<0.001), MPO levels along with significant increased hemoglobin (p<0.01), red blood cell (p<0.05), hematocript(p<0.05) levels and all antioxidant enzymatic activities in plasma and tissues of ceftriaxone plus sulbactam with VRP1034 treated group as compared to cadmium exposed group. δ -aminolevulinic acid dehydratase activity was significantly (p<0.001) increased in the blood of ceftriaxone plus sulbactam with VRP1034 treated group as compared to cadmium exposed group. The levels of hepatic and renal parameters were significantly (p<0.001) decreased in ceftriaxone plus sulbactam with VRP1034 treated group as compared to cadmium exposed group. So these finding concluded that ceftriaxone plus sulbactam with VRP1034 act as potent free radical scavenger and metal chelating properties that reduces free radical mediated tissue injury and prevent hepatic and renal organs dysfunction during cadmium intoxication.
Highlights
Cadmium (Cd) is an industrial and environmental pollutant, arising primarily from battery, electroplating, pigment, plastic, fertilizer industries, and cigarette smoke
Oral administration of cadmium chloride group showed a significant reduction of glutathione reductase enzyme activity in plasma (p
It is transported into the blood and accumulates in the liver where it induces the synthesis of metallothionein (MT), a cytosolic protein to which cadmium binds
Summary
Cadmium (Cd) is an industrial and environmental pollutant, arising primarily from battery, electroplating, pigment, plastic, fertilizer industries, and cigarette smoke. It is dangerous because humans consume both plants and animals that absorb Cd efficiently and concentrate it within their tissues [1]. Chronic exposure to inorganic Cd results in accumulation of the metal mainly in the liver and kidneys, as well as in other tissues and organs causing many metabolic and histological changes, membrane damage, altered gene expression and apoptosis [4,5,6]. A number of cadmiuminduced effects including deterioration of cell-cell adhesion, DNArelated processes; cell signaling and energy metabolism can imply that this metal acts on the different molecular targets in human organs. It is shown that cadmium can induce apoptosis in mouse liver [7]
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
