1. D.

The reactivity of diatomic halogens actually decreases as you move down group 17
of the periodict. Iodine monochloride is very reactive because of the difference in
between iodine and chlorine.
2. B. Li = 1s2, 2s2; Be- = 1s2, 2s2, 2p1 B- =1s2, 2s2, 2p2 ; C- = 1s2, 2s2, 2p3. Be– will be least
stable. It has lowest I.E.
3. C. Lanthanum is a chemical element with symbol La and atomic number 57. It is a soft,
ductile, silvery-white metal that tarnishes rapidly when exposed to air and is soft enough
to be cut with a knife. It is the eponym of the lanthanide series, a group of 15 similar
elements between lanthanum and lutetium in the periodic table, of which lanthanum is the
first and the prototype. It is also sometimes considered the first element of the 6th-period
transition metals and is traditionally counted among the rare earth elements. The usual
oxidation state is +3. Lanthanum has no biological role in humans but is essential to some
bacteria. It is not particularly toxic to humans but does show some antimicrobial activity.
Atomic number (Z) 57
Group 3
Period 6
Block d-block
Electron configuration [Xe] 5d1 6s2
Electrons per shell 2, 8, 18, 18, 9, 2
4. B. Increase the effective nuclear charge so, V+5 has small radius and V+2 has more radius.
Liver diseases remain one of the major health issues which draw a knee interest among the
researcher to develop a therapeutically active formulation with negligible adverse effect. From
last few decades a conclusive clinical study found that tulsi and its active phytoconstituents such
as eugenol and ursolic acid shows hepato-protective effect against various hepatotoxicant such as
heavy metal, paracetamol, chlorpyrifos, carbon tetrachloride and some antitubular drugs.
Alcoholic extract of tulsi protect the liver from cardamium, mercury, and arsenic induced
hepatotoxicity in experimental animals effectively. Administered with tulsi extract ameliorated
hepato-toxicity and decrease the levels of serum transminases, lipid peroxidation and
concomitantly increased the levels of antioxidants (superoxide dismutase), catalase, reduced
glutathione, glutathione peroxidase and Ascorvic acid.

The hepato protective effect of tulsi may be back supported with the decrease level of glutathian
(GSH), glutathian peroxidase. Serum transaminase, lipid peroxidation and can con increase
the level of antioxidant such as superoxide dismutase, super oxide catalase. Antitubular drug
such as isoniazid which metabolized by CYP2E1 to generate a toxic chemical that might be
responsible for hepatotoxicity. Preclinical study signify that co-administering with tulsi extract
dramatically reduced the elevated level of bio-chemical markers such as alanine transaminase,
aspartate transaminase in the serum of the test animal. The histo-pathological analysis signify the
reversal of drug induced hepato-abnormalities like focal necrosis, portal triaditises and steatosis.
Hence a conclusive statement may be considered that to the alcoholic extract of tulsi effectively
increases the hepatic level of GSIT indicating that the protective effect may have been partly
mediated by the increase level of GSH. From the scientific studies it was found that the extract of
tulsi shows the levels of cytokeratin(inflammation), vascular endothelial growth
factor(angiogenesis); proliferating cell nuclear antigen (PCNA), GST Pi(a key protein involved
in proliferation and antiapoptotic protein Bct2 with a simultaneous increase in the pro- apoptotic
proteins BaX, cytochrome C, caspase 3, hepatic antioxidant and GSH.